Camel milk has demonstrated robust immunomodulatory and anti-inflammatory properties in various clinical and experimental studies. However, no previous studies have characterized the cellular immunological effects of camel milk in the context of allergic asthma. Therefore, the present work aimed to evaluate the protective effects of camel milk in house dust mite induced asthma in mice, which emulate human pulmonary inflammation. Female BALB/c mice aged 8- to 10-week-old were intranasally sensitized with vehicle or HDM in 2.5 µl (5 µg) per nostril, 5 days a week for 3 weeks. On day 22, mice received an HDM challenge by a large volume but low dose into the lung (5 µg in 50µl) using intranasal inoculation. Using oral gavage technique, CM/HDM group mice received 0.5 ml of camel milk or vehicle five times a week, starting a day prior to sensitization. On day 23 following HDM challenge, mice were exposed to serial challenges with 10, 20, 40 and 100 mg/ml aerosolized methacholine to measure lung dynamics. Furthermore, BALF and whole lung samples were harvested to examine pulmonary inflammation. Camel milk effectively inhibited both HDM-induced infiltration of eosinophils and AHR. In addition to this, camel milk downregulates the number of pulmonary Th2 and Th17 cells and suppressed CCL17 expression in whole lung homogenates. Furthermore, camel milk reduced HDM-induced IL-4 and IL-13 expression following in vitro restimulation of pulmonary T cell subsets. Additionally, camel milk suppressed total concentrations of IL-5 and IL-13 in the lung. These results corroborate the asthma-preventive potential of camel milk and highlight the significance of diminished local concentrations of Th2- associated cytokines. In the present study, the observed downregulation of asthma progression by camel milk suggests its potential health benefits; however, further experimental and controlled clinical trials are needed before it can be considered a supplementary approach for allergic asthma management.
Copyright: © 2025 Rakhmatulina et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

We previously developed an innovative strategy to induce CD8+ T lymphocyte-immunity through in vivo engineering of extracellular vesicles (EVs). This approach relies on intramuscular injection of DNA expressing antigens of interest fused at a biologically-inactive HIV-1 Nef protein mutant (Nefmut). Nefmut is very efficiently incorporated into EVs, thus conveying large amounts of fusion proteins into EVs released by transfected cells. This platform proved successful against highly immunogenic tumor-specific antigens. Here, we tested whether antigen-specific CD8+ T cell immune responses induced by engineered EVs can counteract the growth of tumors expressing two "self" tumor-associated antigens (TAAs): HOXB7 and Her2/neu. FVB/N mice were injected with DNA vectors expressing Nefmut fused to HOXB7 or Her2/neu, singly and in combination, before subcutaneous implantation of breast carcinoma cells co-expressing HOXB7 and Her2/neu. All mice immunized with the combination vaccine remained tumor-free, whereas groups vaccinated with single Nefmut-fused antigens were only partly protected, with stronger antitumor effects in Her2/neu-immunized mice. Double-vaccinated mice also controlled tumor growth upon a later tumor cell re-challenge. Importantly, co-vaccination also contained tumors in a therapeutic immunization setting. These results showed the efficacy of EV-based vaccination against two TAAs, and represent the first demonstration that HOXB7 may be targeted in multi-antigen immunotherapy strategies.
© 2024. The Author(s).

Inflammatory bowel disease alters the gut microbiota, causes defects in mucosal barrier function, and leads to dysregulation of the immune response to microbial stimulation. This study investigated and compared the efficacy of a candidate probiotic strain, Bacillus coagulans BC198, and its heat-killed form in treating dextran sulfate sodium-induced colitis. Both live and heat-killed B. coagulans BC198 increased gut barrier-associated protein expression, reduced neutrophil and M1 macrophage infiltration of colon tissue, and corrected gut microbial dysbiosis induced by colitis. However, only live B. coagulans BC198 could alleviate the general symptoms of colitis, prevent colon shortening, and suppress inflammation and tissue damage. At the molecular level, live B. coagulans BC198 was able to inhibit Th17 cells while promoting Treg cells in mice with colitis, reduce pro-inflammatory MCP-1 production, and increase anti-inflammatory IL-10 expression in the colonic mucosa. The live form of B. coagulans BC198 functioned more effectively than the heat-killed form in ameliorating colitis by enhancing the anti-inflammatory response and promoting Treg cell accumulation in the colon.
© 2024 The Authors. Published by American Chemical Society.

Dabie bandavirus (DBV) is an emerging tick-borne virus that causes severe fever with thrombocytopenia syndrome (SFTS) in infected patients. Human SFTS symptoms progress from fever, fatigue, and muscle pain to the depletion of white blood cells and platelets with fatality rates up to 30%. The recent spread of its vector tick to over 20 states in the United States increases the potential for outbreaks of the SFTS beyond the East Asia. Thus, the development of vaccine to control this rapidly emerging virus is a high priority. In this study, we applied self-assembling ferritin (FT) nanoparticle to enhance the immunogenicity of DBV Gn head domain (GnH) as a vaccine target. Mice immunized with the GnH-FT nanoparticle vaccine induced potent antibody responses and cellular immunity. Immunized aged ferrets were fully protected from the lethal challenge of DBV. Our study describes the GnH-FT nanoparticle vaccine candidate that provides protective immunity against the emerging DBV infection.

Immunometabolism in the tumor microenvironment (TME) and its influence on the immunotherapy response remain uncertain in colorectal cancer (CRC). We perform immunometabolism subtyping (IMS) on CRC patients in the training and validation cohorts. Three IMS subtypes of CRC, namely, C1, C2, and C3, are identified with distinct immune phenotypes and metabolic properties. The C3 subtype exhibits the poorest prognosis in both the training cohort and the in-house validation cohort. The single-cell transcriptome reveals that a S100A9+ macrophage population contributes to the immunosuppressive TME in C3. The dysfunctional immunotherapy response in the C3 subtype can be reversed by combination treatment with PD-1 blockade and an S100A9 inhibitor tasquinimod. Taken together, we develop an IMS system and identify an immune tolerant C3 subtype that exhibits the poorest prognosis. A multiomics-guided combination strategy by PD-1 blockade and tasquinimod improves responses to immunotherapy by depleting S100A9+ macrophages in vivo.
Copyright © 2023 The Author(s). Published by Elsevier Inc. All rights reserved.