CiteAb

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,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.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 showing Flow cytometry/Cell sorting from the publication: α4-integrins control viral meningoencephalitis through differential recruitment of T helper cell subsets.

Fig.7.P 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.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.

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.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.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.U 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.T 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.R 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.Q 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.M 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.I 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.H 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.E 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.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.

36 images found

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).

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).

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).

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.

Hypoxia activates SREBP2 through Golgi disassembly in bone marrow-derived monocytes for enhanced tumor growth.

In The EMBO Journal on 15 November 2023 by Nakahara, R., Aki, S., et al.

Bone marrow-derived cells (BMDCs) infiltrate hypoxic tumors at a pre-angiogenic state and differentiate into mature macrophages, thereby inducing pro-tumorigenic immunity. A critical factor regulating this differentiation is activation of SREBP2-a well-known transcription factor participating in tumorigenesis progression-through unknown cellular mechanisms. Here, we show that hypoxia-induced Golgi disassembly and Golgi-ER fusion in monocytic myeloid cells result in nuclear translocation and activation of SREBP2 in a SCAP-independent manner. Notably, hypoxia-induced SREBP2 activation was only observed in an immature lineage of bone marrow-derived cells. Single-cell RNA-seq analysis revealed that SREBP2-mediated cholesterol biosynthesis was upregulated in HSCs and monocytes but not in macrophages in the hypoxic bone marrow niche. Moreover, inhibition of cholesterol biosynthesis impaired tumor growth through suppression of pro-tumorigenic immunity and angiogenesis. Thus, our findings indicate that Golgi-ER fusion regulates SREBP2-mediated metabolic alteration in lineage-specific BMDCs under hypoxia for tumor progression.
© 2023 The Authors. Published under the terms of the CC BY NC ND 4.0 license.

View this product on CiteAb

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

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

Collected and cropped from Sci Rep by CiteAb, provided under a CC-BY license

Product Citations: 632

36 images found

Fig.3.C

Fig.2.F

Fig.4.G

Fig.4.E

Fig.4.B

Fig.2.A,B,C,D,E,F,G,H,I,J

Fig.3.J,K,L,M,N,O,P

Fig.2.A

Fig.7.P

Fig.7.A

Fig.7.B

Fig.7.X

Fig.7.V

Fig.7.U

Fig.7.T

Fig.7.R

Fig.7.Q

Fig.7.C

Fig.7.M

Fig.7.L

Fig.7.I

Fig.7.H

Fig.7.F

Fig.7.E

Fig.7.D