Product Citations: 633

Fig.3.A showing Flow cytometry/Cell sorting from the publication: Integrin CD11b negatively regulates Mincle-induced signaling via the Lyn-SIRPα-SHP1 complex.
Fig.5.A showing Flow cytometry/Cell sorting from the publication: Suppressor of Cytokine Signaling 3 in Macrophages Prevents Exacerbated Interleukin-6-Dependent Arginase-1 Activity and Early Permissiveness to Experimental Tuberculosis.
Fig.1.B showing Flow cytometry/Cell sorting from the publication: Suppressor of Cytokine Signaling 3 in Macrophages Prevents Exacerbated Interleukin-6-Dependent Arginase-1 Activity and Early Permissiveness to Experimental Tuberculosis.
Fig.3.C showing Immunohistochemistry-immunofluorescence in a Mus musculus (House mouse) sample from the publication: Leptin sustains spontaneous remyelination in the adult central nervous system.
Fig.2.F showing Immunohistochemistry-immunofluorescence in a Mus musculus (House mouse) sample from the publication: Leptin sustains spontaneous remyelination in the adult central nervous system.
Fig.4.G showing Immunohistochemistry-immunofluorescence in a Mus musculus (House mouse) sample from the publication: Leptin sustains spontaneous remyelination in the adult central nervous system.
Fig.4.E showing Immunohistochemistry in a Rattus norvegicus (Rat) sample from the publication: The impact of chronic intermittent hypoxia on hematopoiesis and the bone marrow microenvironment.
Fig.4.B showing Immunohistochemistry-immunofluorescence in a Mus musculus (House mouse) sample from the publication: Intraperitoneally infused human mesenchymal stem cells form aggregates with mouse immune cells and attach to peritoneal organs.
Fig.2.A showing Flow cytometry/Cell sorting from the publication: MicroRNA-200c Promotes Suppressive Potential of Myeloid-Derived Suppressor Cells by Modulating PTEN and FOG2 Expression.
Fig.3.J,K,L,M,N,O,P showing Immunohistochemistry-immunofluorescence in a Mus musculus (House mouse) sample from the publication: NG2 proteoglycan-dependent recruitment of tumor macrophages promotes pericyte-endothelial cell interactions required for brain tumor vascularization.
Fig.2.A,B,C,D,E,F,G,H,I,J showing Immunohistochemistry-immunofluorescence in a Mus musculus (House mouse) sample from the publication: NG2 proteoglycan-dependent recruitment of tumor macrophages promotes pericyte-endothelial cell interactions required for brain tumor vascularization.
Fig.2.A showing Flow cytometry/Cell sorting from the publication: α4-integrins control viral meningoencephalitis through differential recruitment of T helper cell subsets.
Fig.7.D showing Immunohistochemistry-immunofluorescence in a Mus musculus (House mouse) sample from the publication: IFN-gamma signaling in the central nervous system controls the course of experimental autoimmune encephalomyelitis independently of the localization and composition of inflammatory foci.
Fig.7.F showing Immunohistochemistry-immunofluorescence in a Mus musculus (House mouse) sample from the publication: IFN-gamma signaling in the central nervous system controls the course of experimental autoimmune encephalomyelitis independently of the localization and composition of inflammatory foci.
Fig.7.G showing Immunohistochemistry-immunofluorescence in a Mus musculus (House mouse) sample from the publication: IFN-gamma signaling in the central nervous system controls the course of experimental autoimmune encephalomyelitis independently of the localization and composition of inflammatory foci.
Fig.7.K showing Immunocytochemistry-immunofluorescence in a Mus musculus (House mouse) sample from the publication: IFN-gamma signaling in the central nervous system controls the course of experimental autoimmune encephalomyelitis independently of the localization and composition of inflammatory foci.
Fig.7.L showing Immunocytochemistry-immunofluorescence in a Mus musculus (House mouse) sample from the publication: IFN-gamma signaling in the central nervous system controls the course of experimental autoimmune encephalomyelitis independently of the localization and composition of inflammatory foci.
Fig.7.N showing Immunocytochemistry-immunofluorescence in a Mus musculus (House mouse) sample from the publication: IFN-gamma signaling in the central nervous system controls the course of experimental autoimmune encephalomyelitis independently of the localization and composition of inflammatory foci.
Fig.7.S showing Immunocytochemistry-immunofluorescence in a Mus musculus (House mouse) sample from the publication: IFN-gamma signaling in the central nervous system controls the course of experimental autoimmune encephalomyelitis independently of the localization and composition of inflammatory foci.
Fig.7.V showing Immunohistochemistry-immunofluorescence in a Mus musculus (House mouse) sample from the publication: IFN-gamma signaling in the central nervous system controls the course of experimental autoimmune encephalomyelitis independently of the localization and composition of inflammatory foci.
Fig.7.W showing Immunocytochemistry-immunofluorescence in a Mus musculus (House mouse) sample from the publication: IFN-gamma signaling in the central nervous system controls the course of experimental autoimmune encephalomyelitis independently of the localization and composition of inflammatory foci.
Fig.7.X showing Immunocytochemistry-immunofluorescence in a Mus musculus (House mouse) sample from the publication: IFN-gamma signaling in the central nervous system controls the course of experimental autoimmune encephalomyelitis independently of the localization and composition of inflammatory foci.
Fig.7.C showing Immunohistochemistry-immunofluorescence in a Mus musculus (House mouse) sample from the publication: IFN-gamma signaling in the central nervous system controls the course of experimental autoimmune encephalomyelitis independently of the localization and composition of inflammatory foci.
Fig.7.B showing Immunohistochemistry-immunofluorescence in a Mus musculus (House mouse) sample from the publication: IFN-gamma signaling in the central nervous system controls the course of experimental autoimmune encephalomyelitis independently of the localization and composition of inflammatory foci.
Fig.7.A showing Immunohistochemistry-immunofluorescence in a Mus musculus (House mouse) sample from the publication: IFN-gamma signaling in the central nervous system controls the course of experimental autoimmune encephalomyelitis independently of the localization and composition of inflammatory foci.
40 images found

CD248-targeted BBIR-T cell therapy against late-activated fibroblasts in cardiac repair after myocardial infarction.

In Nature Communications on 27 March 2025 by Chen, H., Hu, K., et al.

Excessive cardiac fibrosis is a key cause of heart failure and adverse ventricular remodeling after myocardial infarction. The abnormally activated fibroblasts after scar maturation are the chief culprit. Single-cell RNA sequencing of mouse cardiac interstitial cells after myocardial infarction depicts a late-activated fibroblast subpopulation F-Act and initially identifies its characteristic antigen CD248, which is also verified in human hearts. On this basis, we develop a CD248-targeted biotin-binding immune receptor T cell therapy against F-Act to correct cardiac repair disorders. In our study, the precise removal of F-Act after the scar matured effectively inhibits fibrotic expansion in the peri-infarct zone and improves cardiac function. This therapy provides an idea for the treatment of cardiac fibrosis and also promotes the application of engineered T cells to non-tumor diseases.
© 2025. The Author(s).

  • Cardiovascular biology
  • Immunology and Microbiology
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Single-cell RNA-seq reveals a resolving immune phenotype in the oral mucosa.

In IScience on 20 September 2024 by Cantalupo, P., Diacou, A., et al.

The oral mucosa is the interface between the host immune response and the oral microbiota. In periodontal disease, the microbial plaque elicits a tissue-destructive immune response. Removal of the microbial stimulus initiates active resolution of inflammatory. Here, we use single-cell RNA-sequencing (scRNA-seq) to characterize the immune response within the oral mucosa across three distinct conditions of periodontal health, disease, and resolution in mice. We report gene expression shifts across the three conditions are driven by macrophage and neutrophils and identify a unique gene signature that characterizes resolution of disease. Macrophage subgroups are identified that demonstrate differential expansion across conditions, including a subgroup that expands during resolution with an immunoregulatory gene signature and enriched for surface marker Cd74. We validate expansion of this subgroup during resolution via flow cytometry. This work presents a robust single-cell dataset of immunological changes in the oral mucosa and identifies a resolution-associated macrophage phenotype in mucosal immunity.
© 2024 The Author(s).

  • Genetics
  • Immunology and Microbiology
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Kupffer cells abrogate homing and repopulation of allogeneic hepatic progenitors in injured liver site.

In Stem Cell Research & Therapy on 20 February 2024 by Abbas, N., You, K., et al.

Allogeneic hepatocyte transplantation is an emerging approach to treat acute liver defects. However, durable engraftment of the transplanted cells remains a daunting task, as they are actively cleared by the recipient's immune system. Therefore, a detailed understanding of the innate or adaptive immune cells-derived responses against allogeneic transplanted hepatic cells is the key to rationalize cell-based therapies.
Here, we induced an acute inflammatory regenerative niche (3-96 h) on the surface of the liver by the application of cryo-injury (CI) to systematically evaluate the innate immune response against transplanted allogeneic hepatic progenitors in a sustained micro-inflammatory environment.
The resulting data highlighted that the injured site was significantly repopulated by alternating numbers of innate immune cells, including neutrophils, monocytes and Kupffer cells (KCs), from 3 to 96 h. The transplanted allo-HPs, engrafted 6 h post-injury, were collectively eliminated by the innate immune response within 24 h of transplantation. Selective depletion of the KCs demonstrated a delayed recruitment of monocytes from day 2 to day 6. In addition, the intrasplenic engraftment of the hepatic progenitors 54 h post-transplantation was dismantled by KCs, while a time-dependent better survival and translocation of the transplanted cells into the injured site could be observed in samples devoid of KCs.
Overall, this study provides evidence that KCs ablation enables a better survival and integration of allo-HPs in a sustained liver inflammatory environment, having implications for rationalizing the cell-based therapeutic interventions against liver defects.
© 2024. The Author(s).

  • Stem Cells and Developmental Biology
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Microglia-mediated drug substance transfer promotes chemoresistance in brain tumors: insights from an in vitro co-culture model using GCV/Tk prodrug system.

In Cancer Cell International on 18 January 2024 by Wu, S. Y., Yu, W. J., et al.

It is well known that tumor-associated macrophages (TAMs) play essential roles in brain tumor resistance to chemotherapy. However, the detailed mechanisms of how TAMs are involved in brain tumor resistance are still unclear and lack a suitable analysis model.
A BV2 microglial cells with ALTS1C1 astrocytoma cells in vitro co-culture system was used to mimic the microglia dominating tumor stroma in the tumor invasion microenvironment and explore the interaction between microglia and brain tumor cells.
Our result suggested that microglia could form colonies with glioma cells under high-density culturing conditions and protect glioma cells from apoptosis induced by chemotherapeutic drugs. Moreover, this study demonstrates that microglia could hijack drug substances from the glioma cells and reduce the drug intensity of ALTS1C1 via direct contact. Inhibition of gap junction protein prevented microglial-glioma colony formation and microglia-mediated chemoresistance.
This study provides novel insights into how glioma cells acquire chemoresistance via microglia-mediated drug substance transferring, providing a new option for treating chemo-resistant brain tumors.
© 2024. The Author(s).

  • Cancer Research
  • Neuroscience
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CD248-targeted BBIR-T cell therapy against late-activated fibroblasts in cardiac repair after myocardial infarction

Preprint on Research Square on 21 November 2023 by Xie, J., Chen, H., et al.

Excessive cardiac fibrosis is a key cause of heart failure and adverse ventricular remodelling after myocardial infarction. The abnormally activated fibroblasts after scar maturation are the chief culprit. Single-cell RNA sequencing of mouse cardiac interstitial cells after myocardial infarction depicts a late-activated fibroblast subpopulation F-Act and initially identifies its characteristic antigen CD248, which is also verified in human hearts. On this basis, we develop a CD248-targeted BBIR-T cell therapy against F-Act to correct cardiac repair disorders. By embedding avidin coupled to the T cell signalling domain onto the membrane, T cells are empowered to recognize and kill target cells labelled by biotinylated antigen-specific molecules. The precise removal of F-Act after the scar matured effectively inhibits fibrotic expansion in the peri-infarct zone and improves cardiac function. This therapy provides a new idea for the treatment of cardiac fibrosis and also promotes the application of engineered T cells to non-tumour diseases.

  • Cardiovascular biology
  • Immunology and Microbiology
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Integrin CD11b negatively regulates Mincle-induced signaling via the Lyn-SIRPα-SHP1 complex.

In Exp Mol Med on 5 February 2018 by Zhang, Q., Lee, W. B., et al.

Fig.3.A
Fig.3.A showing Flow cytometry/Cell sorting from the publication: Integrin CD11b negatively regulates Mincle-induced signaling via the Lyn-SIRPα-SHP1 complex.
  • FC/FACS
CD11b-deficient neutrophils exhibit impaired adhesion but increased activity upon Mincle activation. (a) Bone marrow (BM) neutrophils from WT and CD11b-deficient mice were treated with 50 μg ml−1 TDM, and the surface expression of CD11b and CD18 was determined by flow cytometry 24 h after stimula... more
CD11b-deficient neutrophils exhibit impaired adhesion but increased activity upon Mincle activation. (a) Bone marrow (BM) neutrophils from WT and CD11b-deficient mice were treated with 50 μg ml−1 TDM, and the surface expression of CD11b and CD18 was determined by flow cytometry 24 h after stimulation. (b) WT and CD11b−/− BM neutrophils were prelabeled with calcein acetoxymethyl ester 6 h before treatment with 50 μg ml−1 TDM treatment, with or without priming with 10 ng ml−1 IFN-γ (I+T). Adhered cells were imaged with a fluorescent microscope (bottom panel, × 40). The percentage of adherent cells was determined by measuring the fluorescence with a microplate reader at 492 nm before and after washing (b, top panel). (c) IL-6 and TNF-α levels were assayed 24 h after TDM stimulation. Data are representative of three independent experiments. *P<0.05, **P<0.01, ***P<0.0001 (two-tailed unpaired Student’s t-test). less

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Suppressor of Cytokine Signaling 3 in Macrophages Prevents Exacerbated Interleukin-6-Dependent Arginase-1 Activity and Early Permissiveness to Experimental Tuberculosis.

In Front Immunol on 28 November 2017 by Schmok, E., Abad Dar, M., et al.

Fig.5.A
Fig.5.A showing Flow cytometry/Cell sorting from the publication: Suppressor of Cytokine Signaling 3 in Macrophages Prevents Exacerbated Interleukin-6-Dependent Arginase-1 Activity and Early Permissiveness to Experimental Tuberculosis.
  • FC/FACS
In the absence of macrophage suppressor of cytokine signaling 3 (SOCS3), Mtb infects increasingly arginase-1 (Arg1)-expressing resident macrophages. Cre-negative SOCS3loxP/loxP control mice and LysMcreSOCS3loxP/loxP mice were infected with approximately 1,000 CFU Mtb(A,C) or MtbmCherry(B)via the ... more
In the absence of macrophage suppressor of cytokine signaling 3 (SOCS3), Mtb infects increasingly arginase-1 (Arg1)-expressing resident macrophages. Cre-negative SOCS3loxP/loxP control mice and LysMcreSOCS3loxP/loxP mice were infected with approximately 1,000 CFU Mtb(A,C) or MtbmCherry(B)via the aerosol route. At 21 or 36 days of infection, respectively, perfused lungs were digested and single-cell suspensions were analyzed by flow cytometry for surface expression of CD11b, F4/80, MtbmCherry, and intracellular NOS2 and Arg1. (A,B) For flow cytometric analysis of surface markers, single-cell suspensions of lungs were incubated with an anti-FcγRIII/II monoclonal antibody and stained with optimal concentrations of anti-CD11b and anti-F4/80. (A) Characterization of different macrophage populations (as defined in the representative plot) in SOCS3loxP/loxP and LysMcreSOCS3loxP/loxP mice based on surface expression of CD11b and F4/80. (B) The presence of Mtb in the macrophage populations defined in (A). (C) For intracellular staining of NOS2 and Arg1 in CD11bmed F4/80med and CD11bhi F4/80hi cells isolated from lungs of SOCS3loxP/loxP and LysMcreSOCS3loxP/loxP mice, single-cell suspensions of lungs were stained for surface markers before permeabilization. Staining of NOS2 and Arg1 was performed using optimal concentrations of anti-NOS2 and anti-Arg1 antibodies. Appropriate isotype controls were used. Data represent means ± SD of three to five mice per group. In (A and C), one experiment representative of two performed is shown. less

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Suppressor of Cytokine Signaling 3 in Macrophages Prevents Exacerbated Interleukin-6-Dependent Arginase-1 Activity and Early Permissiveness to Experimental Tuberculosis.

In Front Immunol on 28 November 2017 by Schmok, E., Abad Dar, M., et al.

Fig.1.B
Fig.1.B showing Flow cytometry/Cell sorting from the publication: Suppressor of Cytokine Signaling 3 in Macrophages Prevents Exacerbated Interleukin-6-Dependent Arginase-1 Activity and Early Permissiveness to Experimental Tuberculosis.
  • FC/FACS
Macrophage-specific suppressor of cytokine signaling 3 (SOCS3)-deficient mice were highly susceptible to Mtb infection. Cre-negative SOCS3loxP/loxP control mice (black symbols) and LysMcreSOCS3loxP/loxP mice (white symbols) were infected with approximately 1,000 CFU Mtb via the aerosol route and ... more
Macrophage-specific suppressor of cytokine signaling 3 (SOCS3)-deficient mice were highly susceptible to Mtb infection. Cre-negative SOCS3loxP/loxP control mice (black symbols) and LysMcreSOCS3loxP/loxP mice (white symbols) were infected with approximately 1,000 CFU Mtb via the aerosol route and lungs were isolated at the indicated time points. (A) For mycobacterial colony enumeration assays, aseptically removed lungs were weighed, transferred into PBS containing a proteinase inhibitor cocktail and homogenized. Tenfold serial dilutions of organ homogenates were plated and colonies were counted 3 weeks later. One experiment representative of three performed is shown. (B,C) At 23 days of infection, perfused lungs were digested and single-cell suspensions were analyzed by flow cytometry for surface expression of CD11b and Ly6G (B). (C) After automated cell counting and flow cytometry of CD11b+ F4/80+ macrophages, CD11b+ Ly6G+ granulocytes, and CD4+ T cells, absolute numbers of these cell populations were calculated. Data represent means ± SD of at least five mice per group. One experiment representative of two performed is shown. Statistical analysis was performed as described in experimental procedures defining differences between SOCS3loxP/loxP and LysMcreSOCS3loxP/loxP mice as significant (***p < 0.001; **p < 0.01). (D) Hematoxylin/eosin (H&E, original magnification 100×; scale bar = 1 mm) and Ziehl–Neelsen staining (ZN, original magnification 400×; scale bar = 0.25 mm) of sections from formalin-fixed and paraffin-embedded lungs isolated from mice after 27 days of infection. (E) Survival of 10 infected mice per group was monitored. Animals that lost more than 25% of their original body weight were sacrificed. Statistical analysis was performed as described in experimental procedures defining differences between SOCS3loxP/loxP and LysMcreSOCS3loxP/loxP mice as significant (***p ≤ 0.001). less

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Leptin sustains spontaneous remyelination in the adult central nervous system.

In Sci Rep on 16 January 2017 by Matoba, K., Muramatsu, R., et al.

Fig.3.C
Fig.3.C showing Immunohistochemistry-immunofluorescence in a Mus musculus (House mouse) sample from the publication: Leptin sustains spontaneous remyelination in the adult central nervous system.
  • IHC-IF
  • Mus musculus (House mouse)
Endogenous leptin sustains spontaneous OPC proliferation.(a) Representative images of spinal cord sections, which were prepared 7 days (left panels) and 14 days (right panels) after LPC injection and double labeled for BrdU in combination with PDGFRα (upper panels), GSTπ (upper panels) and olig2 ... more
Endogenous leptin sustains spontaneous OPC proliferation.(a) Representative images of spinal cord sections, which were prepared 7 days (left panels) and 14 days (right panels) after LPC injection and double labeled for BrdU in combination with PDGFRα (upper panels), GSTπ (upper panels) and olig2 (lower panels). BrdU was administrated during 3–7 days after LPC injection; the graph shows quantification (n = 5–8). P = 0.042915 (PDGFRα and BrdU labeled cells), 0.013560 (Olig2 and BrdU labeled cells 7 days after injection), 0.012111 (GSTπ and BrdU labeled cells), 0.009797 (Olig2 and BrdU labeled cells 14 days after injection), Student’s t-test. (b) Representative spinal cord sections, which were prepared 14 days after LPC injection and stained with MBP are shown; the graph shows quantification (n = 6). P = 0.025243, Student’s t-test. (c) Representative images of spinal cord section, which were prepared 7 days after LPC injection and labeled for CD11b; the graph shows quantification (n = 4). P = 0.213763, Student’s t-test, n.s. indicates no significant difference. *P < 0.05, **P < 0.01, error bars represent SEM. Scale bar: 50 μm for high magnification images in a, 100 μm for others. less

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Leptin sustains spontaneous remyelination in the adult central nervous system.

In Sci Rep on 16 January 2017 by Matoba, K., Muramatsu, R., et al.

Fig.2.F
Fig.2.F showing Immunohistochemistry-immunofluorescence in a Mus musculus (House mouse) sample from the publication: Leptin sustains spontaneous remyelination in the adult central nervous system.
  • IHC-IF
  • Mus musculus (House mouse)
LPC injection does not enhance leptin expression in the CNS.(a) Representative images of MBP expression in a mouse spinal cord 14 days after LPC injection are shown; the graph shows quantification of the demyelinating area in the dorsal spinal cord (n = 3–4). P = 0.001542, Student’s t-test. (b) R... more
LPC injection does not enhance leptin expression in the CNS.(a) Representative images of MBP expression in a mouse spinal cord 14 days after LPC injection are shown; the graph shows quantification of the demyelinating area in the dorsal spinal cord (n = 3–4). P = 0.001542, Student’s t-test. (b) Representative images of NeuN expression in a mouse spinal cord 14 days after LPC injection; the graph shows quantification of the density of NeuN-positive cells in the spinal cord (n = 3). P = 0.299940, Student’s t-test, n.s. indicates no significant difference. (c) Quantification of leptin protein expression in indicated organs. Tissues were obtained from the mice 3 days after LPC injection (n = 3 for control, 4 for LPC injection). P = 0.318966 (adipose tissue), 0.10446 (brain stem), 0.332281 (cerebellum), 0.345245 (liver), 0.453104 (kidney), 0.098135 (heart), 0.335722 (lung), 0.236771 (muscle), 0.44662 (spleen), 0.465966 (stomach). Student’s t-test. n.s. indicates no significant difference. (d) Quantification of spinal cord leptin protein 3 days after LPC injection (n = 3 for control, 4 for LPC injection). P = 0.026865, Student’s t-test. (e) Quantification of spinal cord leptin mRNA 3 days after LPC injection (n = 6). P = 0.324930, Student’s t-test, n.s. indicates no significant difference. (f) Representative images of LepRb (green) expression in combination with PDGFRα, GFAP NeuN, and CD11b (red) in the mouse spinal cord with or without LPC injection. Spinal cord sections were obtained 3 days after LPC injection. Graph indicates the relative intensity of leptin protein expression in indicated cell type (n = 3). P = 0.287452 (PDGFRα), 0.181059 (GFAP), 0.199972 (NeuN), Student’s t-test, n.s. indicates no significant difference. *P < 0.05, **P < 0.01, error bars represent SEM. Scale bars; 100 μm for (a and b), 25 μm for (f). less

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Leptin sustains spontaneous remyelination in the adult central nervous system.

In Sci Rep on 16 January 2017 by Matoba, K., Muramatsu, R., et al.

Fig.4.G
Fig.4.G showing Immunohistochemistry-immunofluorescence in a Mus musculus (House mouse) sample from the publication: Leptin sustains spontaneous remyelination in the adult central nervous system.
  • IHC-IF
  • Mus musculus (House mouse)
OPC expresses leptin receptors.(a) Representative images of spinal cord sections, which were double-labeled for LepRb (green) in combination with PDGFRα (red). Spinal cord sections were obtained 7 days after LPC injection; the graph shows quantification (n = 3). P = 0.007573 (LepRb flox vs intact... more
OPC expresses leptin receptors.(a) Representative images of spinal cord sections, which were double-labeled for LepRb (green) in combination with PDGFRα (red). Spinal cord sections were obtained 7 days after LPC injection; the graph shows quantification (n = 3). P = 0.007573 (LepRb flox vs intact CKO), 0.0108779 (LepRb flox vs LPC CKO), ANOVA with Tukey’s post-hoc test. (b) Relative expression of leptin receptors mRNA in PDGFRα-positive OPC obtained from the brain of PDGFRα-creERT:: Lepr flox/flox mice and +/+::Lepr flox/flox mice (n = 5,6). P = 0.005878 (LepRa), 0.010306 (LepRb), 0.001535 (LepRc), 0.003169 (LepRd), 0.030459 (LepRe), Student’s t-test. (c) Representative images of spinal cord sections which were double labeled for BrdU in combination with PDGFRα (left panels) and GSTπ (right panels). Sections were prepared 7 days (left panels) and 14 days (right panels) after LPC injection. BrdU was administrated during 3–7 days after LPC injection; the graph shows quantification (n = 5–8). P = 0.029791(PDGFRα and BrdU labeled cells), 0.028870 (GSTπ and BrdU labeled cells), Student’s t-test. (d) Representative images of PDGFRα expression in the intact spinal cord of PDGFRα-creERT:: Lepr flox/flox mice and +/+::Lepr flox/flox mice; the graph shows quantification (n = 3–4). P = 0.404999, Student’s t-test, n.s. indicates no significant difference. (e) Representative images of APC expression in the intact spinal cord of PDGFRα-creERT:: Lepr flox/flox mice and +/+::Lepr flox/flox mice; the graph shows quantification (n = 3). P = 0.495667, Student’s t-test, n.s. indicates no significant difference. (f) Representative spinal cord section of PDGFRα-creERT:: Lepr flox/flox mice, which were prepared 14 days after LPC injection and stained with MBP; the graph shows quantification of the demyelinating area in the dorsal spinal cord (n = 7 for control, 10 for CKO). P = 0.030688, Student’s t-test. (g) Representative spinal cord sections which were labeled for CD11b. Sections were prepared 7 days after LPC injection. The graph shows quantification (n = 3). P = 0.493264, Student’s t-test, n.s. indicates no significant difference. *P < 0.05, **P < 0.01, error bars represent SEM. Scale bars: 25 μm for (a), 50 μm for high magnification images in (c), 100 μm for others. less

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The impact of chronic intermittent hypoxia on hematopoiesis and the bone marrow microenvironment.

In Pflugers Arch on 1 May 2016 by Alvarez-Martins, I., Remédio, L., et al.

Fig.4.E
Fig.4.E showing Immunohistochemistry in a Rattus norvegicus (Rat) sample from the publication: The impact of chronic intermittent hypoxia on hematopoiesis and the bone marrow microenvironment.
  • IHC
  • Rattus norvegicus (Rat)
Chronic intermittent hypoxia modifies the BM vascular structure. a’–e’ Representative images of femur bone marrow stained with vWF, CD105, VE-cadherin, SMA, and CD11b counterstained with hematoxylin. a”, c”, d” BM from CIH exposed rats (n = 6) has more VE-cadherin+ vessels and SMA coverage but le... more
Chronic intermittent hypoxia modifies the BM vascular structure. a’–e’ Representative images of femur bone marrow stained with vWF, CD105, VE-cadherin, SMA, and CD11b counterstained with hematoxylin. a”, c”, d” BM from CIH exposed rats (n = 6) has more VE-cadherin+ vessels and SMA coverage but less vWF+ sinusoids (400×, Leica DM2500). e’, e” Representative images of CD11b immunohistochemistry in femur BM show an increase in BM monocyte count in CIH exposed animals. (400×, Leica DM2500) a’, a”’, b’, b” No changes in the total number of vessels or in megakaryocyte count were observed, as accounted by CD105 and vWF staining, respectively. Results are represented as the mean ± SD of bone marrow sections from six male Wistar rats (*p < 0.05; **p < 0.01). f Representative images of femur bone marrow fluorescently immunostained for VE-cadherin show an increase in total VE-cadherin vessels and in VE-cadherin vessel coverage. Scale bar, 50 μm (insets magnified 2.5×). Images were acquired with a Zeiss LSM 510 META microscope less

Collected and cropped from Pflugers Arch by CiteAb, provided under a CC-BY license

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Intraperitoneally infused human mesenchymal stem cells form aggregates with mouse immune cells and attach to peritoneal organs.

In Stem Cell Res Ther on 10 February 2016 by Bazhanov, N., Ylöstalo, J. H., et al.

Fig.4.B
Fig.4.B showing Immunohistochemistry-immunofluorescence in a Mus musculus (House mouse) sample from the publication: Intraperitoneally infused human mesenchymal stem cells form aggregates with mouse immune cells and attach to peritoneal organs.
  • IHC-IF
  • Mus musculus (House mouse)
Colocalization of human GFP-MSC with immune cells in the peritoneal cavity. Representative immunofluorescent images of human GFP-MSC in free-floating aggregates, and aggregates attached to the mesentery and omentum 24 h after their IP administration. a In vivo low-magnification (1.5×) images. b G... more
Colocalization of human GFP-MSC with immune cells in the peritoneal cavity. Representative immunofluorescent images of human GFP-MSC in free-floating aggregates, and aggregates attached to the mesentery and omentum 24 h after their IP administration. a In vivo low-magnification (1.5×) images. b GFP-positive aggregates as shown in (a) were obtained from the peritoneal cavity, cryosectioned and stained with CD11b antibody (magnification 20×). c GFP-positive aggregates attached to the mesentery and omentum were isolated with tweezers, fixed, labeled with B220 antibody, and examined as whole mounts (magnification 20×). Representative images from three mice. DAPI 4′,6-Diamidino-2-phenylindole; GFP green fluorescent protein, MSC mesenchymal stem cells less

Collected and cropped from Stem Cell Res Ther by CiteAb, provided under a CC-BY license

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MicroRNA-200c Promotes Suppressive Potential of Myeloid-Derived Suppressor Cells by Modulating PTEN and FOG2 Expression.

In PLoS One on 19 August 2015 by Mei, S., Xin, J., et al.

Fig.2.A
Fig.2.A showing Flow cytometry/Cell sorting from the publication: MicroRNA-200c Promotes Suppressive Potential of Myeloid-Derived Suppressor Cells by Modulating PTEN and FOG2 Expression.
  • FC/FACS
MiR-200c is upregulated by tumor associated GM-CSF.(A) Generation of BM cells derived CD11b+Gr1+ cells. BM cells derived CD11b+Gr1+ cells were generated by culturing with GM-CSF (40 ng/ml) or GM-CSF (40 ng/ml) with IL-6 (40 ng/ml), TNFα (40 ng/ml), or IL-4 (40 ng/ml) plus PGE2 (1.0 μg/ml). The pr... more
MiR-200c is upregulated by tumor associated GM-CSF.(A) Generation of BM cells derived CD11b+Gr1+ cells. BM cells derived CD11b+Gr1+ cells were generated by culturing with GM-CSF (40 ng/ml) or GM-CSF (40 ng/ml) with IL-6 (40 ng/ml), TNFα (40 ng/ml), or IL-4 (40 ng/ml) plus PGE2 (1.0 μg/ml). The proportion of Gr-1+CD11b+ cells was analyzed by FAScan. (B) Expression of miR-200c in differently derived MDSCs. BM cells derived CD11b+Gr1+ cells were generated by culturing with GM-CSF or GM-CSF with IL-6, TNFα, or IL-4 plus PGE2. Total RNAs were isolated from either fresh (fresh) or MDSCs (days 2 or 4 after exposed to the simulators) and miR-200c content was detected by qRT-PCR. Data are normalized to miRNA level in fresh BM cells. (C) Expression of miR-200c in different cytokines treated BM cells. BM cells were treated with different tumor-derived factors GM-CSF, IL-6, TNFα, PGE2 or TGFβ. Ctr., no tumor-derived factor. MiR-200c expression was examined after 24 h. (D) Expression of miR-200c in different doses of GM-CSF treated MDSC. BM cells were cultured with different concentrations of GM-CSF and then expression of miR-200c was analyzed. (E) GM-CSF levels in the supernatants of different tumor cell lines. The tumor supernatants were collected and analyzed by ELISA. (F) Effects of anti-GM-CSF on the expression of miR-200c. BM cells were cultured with 4T1, CT-26 or ID8 TCCM (25% v/v), without or with 10 μg/ml anti-GM-CSF Ab for 36 h. MiR-200c transcriptional levels were detected by qRT-PCR. Ctr., only medium; TCCM, medium with 25% tumor supernatants; TCCM+mAb, medium with 25% tumor supernatants plus anti-murine GM-CSF antibodies. Data are a representative of three independent experiments. *, p<0.05; **, P<0.01. less

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NG2 proteoglycan-dependent recruitment of tumor macrophages promotes pericyte-endothelial cell interactions required for brain tumor vascularization.

In Oncoimmunology on 1 April 2015 by Yotsumoto, F., You, W. K., et al.

Fig.3.J,K,L,M,N,O,P
Fig.3.J,K,L,M,N,O,P showing Immunohistochemistry-immunofluorescence in a Mus musculus (House mouse) sample from the publication: NG2 proteoglycan-dependent recruitment of tumor macrophages promotes pericyte-endothelial cell interactions required for brain tumor vascularization.
  • IHC-IF
  • Mus musculus (House mouse)
NG2-dependent recruitment of bone marrow-derived macrophages. Tumor sections from mice transplanted with EGFP-positive bone marrow from wild type (A–C) or germline NG2 null donors (D–F) were used to localize bone marrow-derived macrophages in relation to CD31-positive blood vessels (red). Panels ... more
NG2-dependent recruitment of bone marrow-derived macrophages. Tumor sections from mice transplanted with EGFP-positive bone marrow from wild type (A–C) or germline NG2 null donors (D–F) were used to localize bone marrow-derived macrophages in relation to CD31-positive blood vessels (red). Panels C and F are merged images of confocal z-stacks. (G) Quantification of EGFP pixels as a percentage of tumor area. In parallel, sections were immunostained for CD11b (red) and for PDGFRβ (not shown) to identify EGFP-positive macrophages and pericytes, respectively, in mice transplanted with EGFP-positive bone marrow from wild type (J–L) or germline NG2 null donors (M–O). Merged images of confocal z-stacks are shown in panels L and O. (H) Quantification of the percentage of EGFP-positive cells that are CD11b-positive. (I) Quantification of the percentage of EGFP-positive cells that are PDGFRβ-positive. Scale bars = 20 μm. *p < 0.01 compared to controls. less

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NG2 proteoglycan-dependent recruitment of tumor macrophages promotes pericyte-endothelial cell interactions required for brain tumor vascularization.

In Oncoimmunology on 1 April 2015 by Yotsumoto, F., You, W. K., et al.

Fig.2.A,B,C,D,E,F,G,H,I,J
Fig.2.A,B,C,D,E,F,G,H,I,J showing Immunohistochemistry-immunofluorescence in a Mus musculus (House mouse) sample from the publication: NG2 proteoglycan-dependent recruitment of tumor macrophages promotes pericyte-endothelial cell interactions required for brain tumor vascularization.
  • IHC-IF
  • Mus musculus (House mouse)
Myeloid-specific NG2 ablation impairs macrophage recruitment to tumors. Double immunostaining for CD11b (blue) and CD31 (green) in tumor sections from control (A–C) and Mac-NG2ko mice (D–F). Areas of overlap in z-stacks appear as pale blue (C,F). Quantification of macrophage abundance in tumors u... more
Myeloid-specific NG2 ablation impairs macrophage recruitment to tumors. Double immunostaining for CD11b (blue) and CD31 (green) in tumor sections from control (A–C) and Mac-NG2ko mice (D–F). Areas of overlap in z-stacks appear as pale blue (C,F). Quantification of macrophage abundance in tumors using the markers F4/80 (G, I) and CD11b (H, J). Data are plotted as the percentage of total tumor area occupied by marker pixels in 10-d tumors (G, H) and 16-day tumors (I, J). Scale bars = 20 μm. *p < 0.01 compared to controls. less

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α4-integrins control viral meningoencephalitis through differential recruitment of T helper cell subsets.

In Acta Neuropathol Commun on 7 March 2014 by Rothhammer, V., Muschaweckh, A., et al.

Fig.2.A
Fig.2.A showing Flow cytometry/Cell sorting from the publication: α4-integrins control viral meningoencephalitis through differential recruitment of T helper cell subsets.
  • FC/FACS
MHC class II positive macrophages are targets of VV infection in the CNS. Wild type mice were infected intrathecally with 1.000 PFUs of VV (eGFP), a replication competent recombinant VV expressing enhanced green fluorescent protein (eGFP) in infected cells. On day 4 after infection, mice were sac... more
MHC class II positive macrophages are targets of VV infection in the CNS. Wild type mice were infected intrathecally with 1.000 PFUs of VV (eGFP), a replication competent recombinant VV expressing enhanced green fluorescent protein (eGFP) in infected cells. On day 4 after infection, mice were sacrificed, and spleen and CNS mononuclear cells were isolated and analyzed by flow cytometry. In the live cell gate, the following populations were defined based on their expression of CD11b and CD45: (A) spleen (SPL), left panel: (1) CD11blowCD45high lymphocytes, (2) CD11bintCD45high dendritic cells, (3) CD11bhighCD45high macrophages. (A) CNS, right panel: (1) CD11blowCD45high lymphocytes, (2) CD11bintCD45int microglia, (3) CD11bhighCD45high macrophages. (B) These populations were analyzed as to their expression of eGFP and MHC class II by flow cytometry. Numbers indicate percentages of positive cells in each quadrant or gate (representative out of 3 independent experiments). less

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IFN-gamma signaling in the central nervous system controls the course of experimental autoimmune encephalomyelitis independently of the localization and composition of inflammatory foci.

In J Neuroinflammation on 16 January 2012 by Lee, E., Chanamara, S., et al.

Fig.7.D
Fig.7.D showing Immunohistochemistry-immunofluorescence in a Mus musculus (House mouse) sample from the publication: IFN-gamma signaling in the central nervous system controls the course of experimental autoimmune encephalomyelitis independently of the localization and composition of inflammatory foci.
  • IHC-IF
  • Mus musculus (House mouse)
STAT1 is mainly expressed in CD11b+ cells. Cerebella and spinal cords isolated from the different groups of mice on day 14 post EAE induction were analyzed for STAT1 expression close to the inflammatory foci and in the normal appearing white or gray matter (NAW/GM). In the CNS of IFNγ-/- mice and... more
STAT1 is mainly expressed in CD11b+ cells. Cerebella and spinal cords isolated from the different groups of mice on day 14 post EAE induction were analyzed for STAT1 expression close to the inflammatory foci and in the normal appearing white or gray matter (NAW/GM). In the CNS of IFNγ-/- mice and IFNγRKO-chimeras STAT1 expression was rarely detected, while CD11b+ cells were abundant both in the cerebellum and spinal cord (A-D, I-L). STAT1 expression was readily detectable in the CNS of WT mice and WT-chimeras both within the inflammatory foci (E, G, Q and S) and in the NAW/GM (F, H, R and T). In IFNγRCNSKO mice, STAT1 expression was prominent in CD11b+ cells within the inflammatory foci (M, O), while it was rarely detected in CD11b+ cells with ramified morphology away from the inflammatory lesions (N, P). In the CNS of IFNγRperiKO mice, the majority of CD11b+ cells with amoeboid morphology (activated microglia or macrophages) in the inflammatory foci did not express STAT1 (U, W). STAT1 was mainly expressed by CD11b+ cells located in the normal appearing gray matter, exhibiting morphology similar to that of ramified microglia (V, X). Space bar = 50 μm. Inserts show selected magnified fields to confirm STAT1 upregulation. Space bar = 10 μm. Nuclei were visualized by DAPI staining. Two (out of 4-6) representative mice per set are shown. less

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IFN-gamma signaling in the central nervous system controls the course of experimental autoimmune encephalomyelitis independently of the localization and composition of inflammatory foci.

In J Neuroinflammation on 16 January 2012 by Lee, E., Chanamara, S., et al.

Fig.7.F
Fig.7.F showing Immunohistochemistry-immunofluorescence in a Mus musculus (House mouse) sample from the publication: IFN-gamma signaling in the central nervous system controls the course of experimental autoimmune encephalomyelitis independently of the localization and composition of inflammatory foci.
  • IHC-IF
  • Mus musculus (House mouse)
STAT1 is mainly expressed in CD11b+ cells. Cerebella and spinal cords isolated from the different groups of mice on day 14 post EAE induction were analyzed for STAT1 expression close to the inflammatory foci and in the normal appearing white or gray matter (NAW/GM). In the CNS of IFNγ-/- mice and... more
STAT1 is mainly expressed in CD11b+ cells. Cerebella and spinal cords isolated from the different groups of mice on day 14 post EAE induction were analyzed for STAT1 expression close to the inflammatory foci and in the normal appearing white or gray matter (NAW/GM). In the CNS of IFNγ-/- mice and IFNγRKO-chimeras STAT1 expression was rarely detected, while CD11b+ cells were abundant both in the cerebellum and spinal cord (A-D, I-L). STAT1 expression was readily detectable in the CNS of WT mice and WT-chimeras both within the inflammatory foci (E, G, Q and S) and in the NAW/GM (F, H, R and T). In IFNγRCNSKO mice, STAT1 expression was prominent in CD11b+ cells within the inflammatory foci (M, O), while it was rarely detected in CD11b+ cells with ramified morphology away from the inflammatory lesions (N, P). In the CNS of IFNγRperiKO mice, the majority of CD11b+ cells with amoeboid morphology (activated microglia or macrophages) in the inflammatory foci did not express STAT1 (U, W). STAT1 was mainly expressed by CD11b+ cells located in the normal appearing gray matter, exhibiting morphology similar to that of ramified microglia (V, X). Space bar = 50 μm. Inserts show selected magnified fields to confirm STAT1 upregulation. Space bar = 10 μm. Nuclei were visualized by DAPI staining. Two (out of 4-6) representative mice per set are shown. less

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IFN-gamma signaling in the central nervous system controls the course of experimental autoimmune encephalomyelitis independently of the localization and composition of inflammatory foci.

In J Neuroinflammation on 16 January 2012 by Lee, E., Chanamara, S., et al.

Fig.7.G
Fig.7.G showing Immunohistochemistry-immunofluorescence in a Mus musculus (House mouse) sample from the publication: IFN-gamma signaling in the central nervous system controls the course of experimental autoimmune encephalomyelitis independently of the localization and composition of inflammatory foci.
  • IHC-IF
  • Mus musculus (House mouse)
STAT1 is mainly expressed in CD11b+ cells. Cerebella and spinal cords isolated from the different groups of mice on day 14 post EAE induction were analyzed for STAT1 expression close to the inflammatory foci and in the normal appearing white or gray matter (NAW/GM). In the CNS of IFNγ-/- mice and... more
STAT1 is mainly expressed in CD11b+ cells. Cerebella and spinal cords isolated from the different groups of mice on day 14 post EAE induction were analyzed for STAT1 expression close to the inflammatory foci and in the normal appearing white or gray matter (NAW/GM). In the CNS of IFNγ-/- mice and IFNγRKO-chimeras STAT1 expression was rarely detected, while CD11b+ cells were abundant both in the cerebellum and spinal cord (A-D, I-L). STAT1 expression was readily detectable in the CNS of WT mice and WT-chimeras both within the inflammatory foci (E, G, Q and S) and in the NAW/GM (F, H, R and T). In IFNγRCNSKO mice, STAT1 expression was prominent in CD11b+ cells within the inflammatory foci (M, O), while it was rarely detected in CD11b+ cells with ramified morphology away from the inflammatory lesions (N, P). In the CNS of IFNγRperiKO mice, the majority of CD11b+ cells with amoeboid morphology (activated microglia or macrophages) in the inflammatory foci did not express STAT1 (U, W). STAT1 was mainly expressed by CD11b+ cells located in the normal appearing gray matter, exhibiting morphology similar to that of ramified microglia (V, X). Space bar = 50 μm. Inserts show selected magnified fields to confirm STAT1 upregulation. Space bar = 10 μm. Nuclei were visualized by DAPI staining. Two (out of 4-6) representative mice per set are shown. less

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IFN-gamma signaling in the central nervous system controls the course of experimental autoimmune encephalomyelitis independently of the localization and composition of inflammatory foci.

In J Neuroinflammation on 16 January 2012 by Lee, E., Chanamara, S., et al.

Fig.7.K
Fig.7.K showing Immunocytochemistry-immunofluorescence in a Mus musculus (House mouse) sample from the publication: IFN-gamma signaling in the central nervous system controls the course of experimental autoimmune encephalomyelitis independently of the localization and composition of inflammatory foci.
  • ICC-IF
  • Mus musculus (House mouse)
STAT1 is mainly expressed in CD11b+ cells. Cerebella and spinal cords isolated from the different groups of mice on day 14 post EAE induction were analyzed for STAT1 expression close to the inflammatory foci and in the normal appearing white or gray matter (NAW/GM). In the CNS of IFNγ-/- mice and... more
STAT1 is mainly expressed in CD11b+ cells. Cerebella and spinal cords isolated from the different groups of mice on day 14 post EAE induction were analyzed for STAT1 expression close to the inflammatory foci and in the normal appearing white or gray matter (NAW/GM). In the CNS of IFNγ-/- mice and IFNγRKO-chimeras STAT1 expression was rarely detected, while CD11b+ cells were abundant both in the cerebellum and spinal cord (A-D, I-L). STAT1 expression was readily detectable in the CNS of WT mice and WT-chimeras both within the inflammatory foci (E, G, Q and S) and in the NAW/GM (F, H, R and T). In IFNγRCNSKO mice, STAT1 expression was prominent in CD11b+ cells within the inflammatory foci (M, O), while it was rarely detected in CD11b+ cells with ramified morphology away from the inflammatory lesions (N, P). In the CNS of IFNγRperiKO mice, the majority of CD11b+ cells with amoeboid morphology (activated microglia or macrophages) in the inflammatory foci did not express STAT1 (U, W). STAT1 was mainly expressed by CD11b+ cells located in the normal appearing gray matter, exhibiting morphology similar to that of ramified microglia (V, X). Space bar = 50 μm. Inserts show selected magnified fields to confirm STAT1 upregulation. Space bar = 10 μm. Nuclei were visualized by DAPI staining. Two (out of 4-6) representative mice per set are shown. less

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IFN-gamma signaling in the central nervous system controls the course of experimental autoimmune encephalomyelitis independently of the localization and composition of inflammatory foci.

In J Neuroinflammation on 16 January 2012 by Lee, E., Chanamara, S., et al.

Fig.7.L
Fig.7.L showing Immunocytochemistry-immunofluorescence in a Mus musculus (House mouse) sample from the publication: IFN-gamma signaling in the central nervous system controls the course of experimental autoimmune encephalomyelitis independently of the localization and composition of inflammatory foci.
  • ICC-IF
  • Mus musculus (House mouse)
STAT1 is mainly expressed in CD11b+ cells. Cerebella and spinal cords isolated from the different groups of mice on day 14 post EAE induction were analyzed for STAT1 expression close to the inflammatory foci and in the normal appearing white or gray matter (NAW/GM). In the CNS of IFNγ-/- mice and... more
STAT1 is mainly expressed in CD11b+ cells. Cerebella and spinal cords isolated from the different groups of mice on day 14 post EAE induction were analyzed for STAT1 expression close to the inflammatory foci and in the normal appearing white or gray matter (NAW/GM). In the CNS of IFNγ-/- mice and IFNγRKO-chimeras STAT1 expression was rarely detected, while CD11b+ cells were abundant both in the cerebellum and spinal cord (A-D, I-L). STAT1 expression was readily detectable in the CNS of WT mice and WT-chimeras both within the inflammatory foci (E, G, Q and S) and in the NAW/GM (F, H, R and T). In IFNγRCNSKO mice, STAT1 expression was prominent in CD11b+ cells within the inflammatory foci (M, O), while it was rarely detected in CD11b+ cells with ramified morphology away from the inflammatory lesions (N, P). In the CNS of IFNγRperiKO mice, the majority of CD11b+ cells with amoeboid morphology (activated microglia or macrophages) in the inflammatory foci did not express STAT1 (U, W). STAT1 was mainly expressed by CD11b+ cells located in the normal appearing gray matter, exhibiting morphology similar to that of ramified microglia (V, X). Space bar = 50 μm. Inserts show selected magnified fields to confirm STAT1 upregulation. Space bar = 10 μm. Nuclei were visualized by DAPI staining. Two (out of 4-6) representative mice per set are shown. less

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IFN-gamma signaling in the central nervous system controls the course of experimental autoimmune encephalomyelitis independently of the localization and composition of inflammatory foci.

In J Neuroinflammation on 16 January 2012 by Lee, E., Chanamara, S., et al.

Fig.7.N
Fig.7.N showing Immunocytochemistry-immunofluorescence in a Mus musculus (House mouse) sample from the publication: IFN-gamma signaling in the central nervous system controls the course of experimental autoimmune encephalomyelitis independently of the localization and composition of inflammatory foci.
  • ICC-IF
  • Mus musculus (House mouse)
STAT1 is mainly expressed in CD11b+ cells. Cerebella and spinal cords isolated from the different groups of mice on day 14 post EAE induction were analyzed for STAT1 expression close to the inflammatory foci and in the normal appearing white or gray matter (NAW/GM). In the CNS of IFNγ-/- mice and... more
STAT1 is mainly expressed in CD11b+ cells. Cerebella and spinal cords isolated from the different groups of mice on day 14 post EAE induction were analyzed for STAT1 expression close to the inflammatory foci and in the normal appearing white or gray matter (NAW/GM). In the CNS of IFNγ-/- mice and IFNγRKO-chimeras STAT1 expression was rarely detected, while CD11b+ cells were abundant both in the cerebellum and spinal cord (A-D, I-L). STAT1 expression was readily detectable in the CNS of WT mice and WT-chimeras both within the inflammatory foci (E, G, Q and S) and in the NAW/GM (F, H, R and T). In IFNγRCNSKO mice, STAT1 expression was prominent in CD11b+ cells within the inflammatory foci (M, O), while it was rarely detected in CD11b+ cells with ramified morphology away from the inflammatory lesions (N, P). In the CNS of IFNγRperiKO mice, the majority of CD11b+ cells with amoeboid morphology (activated microglia or macrophages) in the inflammatory foci did not express STAT1 (U, W). STAT1 was mainly expressed by CD11b+ cells located in the normal appearing gray matter, exhibiting morphology similar to that of ramified microglia (V, X). Space bar = 50 μm. Inserts show selected magnified fields to confirm STAT1 upregulation. Space bar = 10 μm. Nuclei were visualized by DAPI staining. Two (out of 4-6) representative mice per set are shown. less

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IFN-gamma signaling in the central nervous system controls the course of experimental autoimmune encephalomyelitis independently of the localization and composition of inflammatory foci.

In J Neuroinflammation on 16 January 2012 by Lee, E., Chanamara, S., et al.

Fig.7.S
Fig.7.S showing Immunocytochemistry-immunofluorescence in a Mus musculus (House mouse) sample from the publication: IFN-gamma signaling in the central nervous system controls the course of experimental autoimmune encephalomyelitis independently of the localization and composition of inflammatory foci.
  • ICC-IF
  • Mus musculus (House mouse)
STAT1 is mainly expressed in CD11b+ cells. Cerebella and spinal cords isolated from the different groups of mice on day 14 post EAE induction were analyzed for STAT1 expression close to the inflammatory foci and in the normal appearing white or gray matter (NAW/GM). In the CNS of IFNγ-/- mice and... more
STAT1 is mainly expressed in CD11b+ cells. Cerebella and spinal cords isolated from the different groups of mice on day 14 post EAE induction were analyzed for STAT1 expression close to the inflammatory foci and in the normal appearing white or gray matter (NAW/GM). In the CNS of IFNγ-/- mice and IFNγRKO-chimeras STAT1 expression was rarely detected, while CD11b+ cells were abundant both in the cerebellum and spinal cord (A-D, I-L). STAT1 expression was readily detectable in the CNS of WT mice and WT-chimeras both within the inflammatory foci (E, G, Q and S) and in the NAW/GM (F, H, R and T). In IFNγRCNSKO mice, STAT1 expression was prominent in CD11b+ cells within the inflammatory foci (M, O), while it was rarely detected in CD11b+ cells with ramified morphology away from the inflammatory lesions (N, P). In the CNS of IFNγRperiKO mice, the majority of CD11b+ cells with amoeboid morphology (activated microglia or macrophages) in the inflammatory foci did not express STAT1 (U, W). STAT1 was mainly expressed by CD11b+ cells located in the normal appearing gray matter, exhibiting morphology similar to that of ramified microglia (V, X). Space bar = 50 μm. Inserts show selected magnified fields to confirm STAT1 upregulation. Space bar = 10 μm. Nuclei were visualized by DAPI staining. Two (out of 4-6) representative mice per set are shown. less

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IFN-gamma signaling in the central nervous system controls the course of experimental autoimmune encephalomyelitis independently of the localization and composition of inflammatory foci.

In J Neuroinflammation on 16 January 2012 by Lee, E., Chanamara, S., et al.

Fig.7.V
Fig.7.V showing Immunohistochemistry-immunofluorescence in a Mus musculus (House mouse) sample from the publication: IFN-gamma signaling in the central nervous system controls the course of experimental autoimmune encephalomyelitis independently of the localization and composition of inflammatory foci.
  • IHC-IF
  • Mus musculus (House mouse)
STAT1 is mainly expressed in CD11b+ cells. Cerebella and spinal cords isolated from the different groups of mice on day 14 post EAE induction were analyzed for STAT1 expression close to the inflammatory foci and in the normal appearing white or gray matter (NAW/GM). In the CNS of IFNγ-/- mice and... more
STAT1 is mainly expressed in CD11b+ cells. Cerebella and spinal cords isolated from the different groups of mice on day 14 post EAE induction were analyzed for STAT1 expression close to the inflammatory foci and in the normal appearing white or gray matter (NAW/GM). In the CNS of IFNγ-/- mice and IFNγRKO-chimeras STAT1 expression was rarely detected, while CD11b+ cells were abundant both in the cerebellum and spinal cord (A-D, I-L). STAT1 expression was readily detectable in the CNS of WT mice and WT-chimeras both within the inflammatory foci (E, G, Q and S) and in the NAW/GM (F, H, R and T). In IFNγRCNSKO mice, STAT1 expression was prominent in CD11b+ cells within the inflammatory foci (M, O), while it was rarely detected in CD11b+ cells with ramified morphology away from the inflammatory lesions (N, P). In the CNS of IFNγRperiKO mice, the majority of CD11b+ cells with amoeboid morphology (activated microglia or macrophages) in the inflammatory foci did not express STAT1 (U, W). STAT1 was mainly expressed by CD11b+ cells located in the normal appearing gray matter, exhibiting morphology similar to that of ramified microglia (V, X). Space bar = 50 μm. Inserts show selected magnified fields to confirm STAT1 upregulation. Space bar = 10 μm. Nuclei were visualized by DAPI staining. Two (out of 4-6) representative mice per set are shown. less

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IFN-gamma signaling in the central nervous system controls the course of experimental autoimmune encephalomyelitis independently of the localization and composition of inflammatory foci.

In J Neuroinflammation on 16 January 2012 by Lee, E., Chanamara, S., et al.

Fig.7.W
Fig.7.W showing Immunocytochemistry-immunofluorescence in a Mus musculus (House mouse) sample from the publication: IFN-gamma signaling in the central nervous system controls the course of experimental autoimmune encephalomyelitis independently of the localization and composition of inflammatory foci.
  • ICC-IF
  • Mus musculus (House mouse)
STAT1 is mainly expressed in CD11b+ cells. Cerebella and spinal cords isolated from the different groups of mice on day 14 post EAE induction were analyzed for STAT1 expression close to the inflammatory foci and in the normal appearing white or gray matter (NAW/GM). In the CNS of IFNγ-/- mice and... more
STAT1 is mainly expressed in CD11b+ cells. Cerebella and spinal cords isolated from the different groups of mice on day 14 post EAE induction were analyzed for STAT1 expression close to the inflammatory foci and in the normal appearing white or gray matter (NAW/GM). In the CNS of IFNγ-/- mice and IFNγRKO-chimeras STAT1 expression was rarely detected, while CD11b+ cells were abundant both in the cerebellum and spinal cord (A-D, I-L). STAT1 expression was readily detectable in the CNS of WT mice and WT-chimeras both within the inflammatory foci (E, G, Q and S) and in the NAW/GM (F, H, R and T). In IFNγRCNSKO mice, STAT1 expression was prominent in CD11b+ cells within the inflammatory foci (M, O), while it was rarely detected in CD11b+ cells with ramified morphology away from the inflammatory lesions (N, P). In the CNS of IFNγRperiKO mice, the majority of CD11b+ cells with amoeboid morphology (activated microglia or macrophages) in the inflammatory foci did not express STAT1 (U, W). STAT1 was mainly expressed by CD11b+ cells located in the normal appearing gray matter, exhibiting morphology similar to that of ramified microglia (V, X). Space bar = 50 μm. Inserts show selected magnified fields to confirm STAT1 upregulation. Space bar = 10 μm. Nuclei were visualized by DAPI staining. Two (out of 4-6) representative mice per set are shown. less

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IFN-gamma signaling in the central nervous system controls the course of experimental autoimmune encephalomyelitis independently of the localization and composition of inflammatory foci.

In J Neuroinflammation on 16 January 2012 by Lee, E., Chanamara, S., et al.

Fig.7.X
Fig.7.X showing Immunocytochemistry-immunofluorescence in a Mus musculus (House mouse) sample from the publication: IFN-gamma signaling in the central nervous system controls the course of experimental autoimmune encephalomyelitis independently of the localization and composition of inflammatory foci.
  • ICC-IF
  • Mus musculus (House mouse)
STAT1 is mainly expressed in CD11b+ cells. Cerebella and spinal cords isolated from the different groups of mice on day 14 post EAE induction were analyzed for STAT1 expression close to the inflammatory foci and in the normal appearing white or gray matter (NAW/GM). In the CNS of IFNγ-/- mice and... more
STAT1 is mainly expressed in CD11b+ cells. Cerebella and spinal cords isolated from the different groups of mice on day 14 post EAE induction were analyzed for STAT1 expression close to the inflammatory foci and in the normal appearing white or gray matter (NAW/GM). In the CNS of IFNγ-/- mice and IFNγRKO-chimeras STAT1 expression was rarely detected, while CD11b+ cells were abundant both in the cerebellum and spinal cord (A-D, I-L). STAT1 expression was readily detectable in the CNS of WT mice and WT-chimeras both within the inflammatory foci (E, G, Q and S) and in the NAW/GM (F, H, R and T). In IFNγRCNSKO mice, STAT1 expression was prominent in CD11b+ cells within the inflammatory foci (M, O), while it was rarely detected in CD11b+ cells with ramified morphology away from the inflammatory lesions (N, P). In the CNS of IFNγRperiKO mice, the majority of CD11b+ cells with amoeboid morphology (activated microglia or macrophages) in the inflammatory foci did not express STAT1 (U, W). STAT1 was mainly expressed by CD11b+ cells located in the normal appearing gray matter, exhibiting morphology similar to that of ramified microglia (V, X). Space bar = 50 μm. Inserts show selected magnified fields to confirm STAT1 upregulation. Space bar = 10 μm. Nuclei were visualized by DAPI staining. Two (out of 4-6) representative mice per set are shown. less

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IFN-gamma signaling in the central nervous system controls the course of experimental autoimmune encephalomyelitis independently of the localization and composition of inflammatory foci.

In J Neuroinflammation on 16 January 2012 by Lee, E., Chanamara, S., et al.

Fig.7.C
Fig.7.C showing Immunohistochemistry-immunofluorescence in a Mus musculus (House mouse) sample from the publication: IFN-gamma signaling in the central nervous system controls the course of experimental autoimmune encephalomyelitis independently of the localization and composition of inflammatory foci.
  • IHC-IF
  • Mus musculus (House mouse)
STAT1 is mainly expressed in CD11b+ cells. Cerebella and spinal cords isolated from the different groups of mice on day 14 post EAE induction were analyzed for STAT1 expression close to the inflammatory foci and in the normal appearing white or gray matter (NAW/GM). In the CNS of IFNγ-/- mice and... more
STAT1 is mainly expressed in CD11b+ cells. Cerebella and spinal cords isolated from the different groups of mice on day 14 post EAE induction were analyzed for STAT1 expression close to the inflammatory foci and in the normal appearing white or gray matter (NAW/GM). In the CNS of IFNγ-/- mice and IFNγRKO-chimeras STAT1 expression was rarely detected, while CD11b+ cells were abundant both in the cerebellum and spinal cord (A-D, I-L). STAT1 expression was readily detectable in the CNS of WT mice and WT-chimeras both within the inflammatory foci (E, G, Q and S) and in the NAW/GM (F, H, R and T). In IFNγRCNSKO mice, STAT1 expression was prominent in CD11b+ cells within the inflammatory foci (M, O), while it was rarely detected in CD11b+ cells with ramified morphology away from the inflammatory lesions (N, P). In the CNS of IFNγRperiKO mice, the majority of CD11b+ cells with amoeboid morphology (activated microglia or macrophages) in the inflammatory foci did not express STAT1 (U, W). STAT1 was mainly expressed by CD11b+ cells located in the normal appearing gray matter, exhibiting morphology similar to that of ramified microglia (V, X). Space bar = 50 μm. Inserts show selected magnified fields to confirm STAT1 upregulation. Space bar = 10 μm. Nuclei were visualized by DAPI staining. Two (out of 4-6) representative mice per set are shown. less

Collected and cropped from J Neuroinflammation by CiteAb, provided under a CC-BY license

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IFN-gamma signaling in the central nervous system controls the course of experimental autoimmune encephalomyelitis independently of the localization and composition of inflammatory foci.

In J Neuroinflammation on 16 January 2012 by Lee, E., Chanamara, S., et al.

Fig.7.B
Fig.7.B showing Immunohistochemistry-immunofluorescence in a Mus musculus (House mouse) sample from the publication: IFN-gamma signaling in the central nervous system controls the course of experimental autoimmune encephalomyelitis independently of the localization and composition of inflammatory foci.
  • IHC-IF
  • Mus musculus (House mouse)
STAT1 is mainly expressed in CD11b+ cells. Cerebella and spinal cords isolated from the different groups of mice on day 14 post EAE induction were analyzed for STAT1 expression close to the inflammatory foci and in the normal appearing white or gray matter (NAW/GM). In the CNS of IFNγ-/- mice and... more
STAT1 is mainly expressed in CD11b+ cells. Cerebella and spinal cords isolated from the different groups of mice on day 14 post EAE induction were analyzed for STAT1 expression close to the inflammatory foci and in the normal appearing white or gray matter (NAW/GM). In the CNS of IFNγ-/- mice and IFNγRKO-chimeras STAT1 expression was rarely detected, while CD11b+ cells were abundant both in the cerebellum and spinal cord (A-D, I-L). STAT1 expression was readily detectable in the CNS of WT mice and WT-chimeras both within the inflammatory foci (E, G, Q and S) and in the NAW/GM (F, H, R and T). In IFNγRCNSKO mice, STAT1 expression was prominent in CD11b+ cells within the inflammatory foci (M, O), while it was rarely detected in CD11b+ cells with ramified morphology away from the inflammatory lesions (N, P). In the CNS of IFNγRperiKO mice, the majority of CD11b+ cells with amoeboid morphology (activated microglia or macrophages) in the inflammatory foci did not express STAT1 (U, W). STAT1 was mainly expressed by CD11b+ cells located in the normal appearing gray matter, exhibiting morphology similar to that of ramified microglia (V, X). Space bar = 50 μm. Inserts show selected magnified fields to confirm STAT1 upregulation. Space bar = 10 μm. Nuclei were visualized by DAPI staining. Two (out of 4-6) representative mice per set are shown. less

Collected and cropped from J Neuroinflammation by CiteAb, provided under a CC-BY license

View on PubMed®

Image 1 of 40

IFN-gamma signaling in the central nervous system controls the course of experimental autoimmune encephalomyelitis independently of the localization and composition of inflammatory foci.

In J Neuroinflammation on 16 January 2012 by Lee, E., Chanamara, S., et al.

Fig.7.A
Fig.7.A showing Immunohistochemistry-immunofluorescence in a Mus musculus (House mouse) sample from the publication: IFN-gamma signaling in the central nervous system controls the course of experimental autoimmune encephalomyelitis independently of the localization and composition of inflammatory foci.
  • IHC-IF
  • Mus musculus (House mouse)
STAT1 is mainly expressed in CD11b+ cells. Cerebella and spinal cords isolated from the different groups of mice on day 14 post EAE induction were analyzed for STAT1 expression close to the inflammatory foci and in the normal appearing white or gray matter (NAW/GM). In the CNS of IFNγ-/- mice and... more
STAT1 is mainly expressed in CD11b+ cells. Cerebella and spinal cords isolated from the different groups of mice on day 14 post EAE induction were analyzed for STAT1 expression close to the inflammatory foci and in the normal appearing white or gray matter (NAW/GM). In the CNS of IFNγ-/- mice and IFNγRKO-chimeras STAT1 expression was rarely detected, while CD11b+ cells were abundant both in the cerebellum and spinal cord (A-D, I-L). STAT1 expression was readily detectable in the CNS of WT mice and WT-chimeras both within the inflammatory foci (E, G, Q and S) and in the NAW/GM (F, H, R and T). In IFNγRCNSKO mice, STAT1 expression was prominent in CD11b+ cells within the inflammatory foci (M, O), while it was rarely detected in CD11b+ cells with ramified morphology away from the inflammatory lesions (N, P). In the CNS of IFNγRperiKO mice, the majority of CD11b+ cells with amoeboid morphology (activated microglia or macrophages) in the inflammatory foci did not express STAT1 (U, W). STAT1 was mainly expressed by CD11b+ cells located in the normal appearing gray matter, exhibiting morphology similar to that of ramified microglia (V, X). Space bar = 50 μm. Inserts show selected magnified fields to confirm STAT1 upregulation. Space bar = 10 μm. Nuclei were visualized by DAPI staining. Two (out of 4-6) representative mice per set are shown. less

Collected and cropped from J Neuroinflammation by CiteAb, provided under a CC-BY license

View on PubMed®

Image 1 of 40