Several factors contribute to the maintenance of central nervous system immune privilege and astrocytes have been identified as a major source of immunomodulatory cytokines. To investigate whether hematogenous monocytes are immunologically deactivated by astrocyte-derived factors human monocytes were stimulated with lipopolysaccharide or interferon (IFN)-gamma and treated with the supernatant from pure astrocyte cultures, interleukin (IL)-4, IL-10, or with IL-1-receptor antagonist (1L-1-RA). Flow cytometry demonstrated that the supernatant from astrocyte cultures was the most potent agent in reducing the levels of major histocompatibility complex (MHC)-class-II- as well as intercellular adhesion molecule-1-expression, whereas IL-4, IL-10, and IL-1-RA had only marginal effects. The expression of leukocyte function antigen-1 and very late antigen-4 was not modulated by either factor. In conclusion, astrocytes seem to provide soluble factors that have the capacity to deactivate hematogenous monocytes.
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http://dx.doi.org/10.1016/s0304-3940(00)01711-0 | DOI Listing |
Front Immunol
January 2025
Institute of Translational Medicine, Medical College, Yangzhou University, Yangzhou, China.
NPJ Syst Biol Appl
January 2025
Department of Immunology, University of Pittsburgh, Pittsburgh, PA, USA.
T cells mediate pathogenesis of several autoimmune disorders by recognizing self-epitopes presented on Major Histocompatibility Complex (MHC) or Human Leukocyte Antigen (HLA) complex. The majority of autoantigens presented to T cells in various autoimmune disorders are not known, which has impeded autoantigen identification. Recent advances in immunopeptidomics have started to unravel the repertoire of antigenic epitopes presented on MHC.
View Article and Find Full Text PDFGenomics Proteomics Bioinformatics
January 2025
Center for Epigenetics and Disease Prevention, Institute of Biosciences and Technology, Texas A&M University, Houston, TX 77030, USA.
Tumor-specific antigens, also known as neoantigens, have potential utility in anti-cancer immunotherapy, including immune checkpoint blockade (ICB), neoantigen-specific T cell receptor-engineered T (TCR-T), chimeric antigen receptor T (CAR-T), and therapeutic cancer vaccines (TCVs). After recognizing presented neoantigens, the immune system becomes activated and triggers the death of tumor cells. Neoantigens may be derived from multiple origins, including somatic mutations (single nucleotide variants, insertion/deletions, and gene fusions), circular RNAs, alternative splicing, RNA editing, and polymorphic microbiome.
View Article and Find Full Text PDFTranspl Int
January 2025
Department of Chronic Diseases, Metabolism and Ageing, Laboratory for Respiratory Diseases and Thoracic Surgery, Faculty of Medicine, KU Leuven, Leuven, Belgium.
Lung transplantation is a life-saving therapeutic option for many chronic end-stage pulmonary diseases, but long-term survival may be limited by rejection of the transplanted organ. Since HLA disparity between donor and recipient plays a major role in rejection, we performed a single center, retrospective observational cohort analysis in our lung transplant cohort (n = 128) in which we calculated HLA compatibility scores for B-cell epitopes (HLAMatchmaker, HLA-EMMA), T-cell epitopes (PIRCHE-II) and missing self-induced NK cell activation (KIR Ligand Calculator). Adjusted Cox proportional hazards model was used to investigate the association between mismatched scores and time to development of donor-specific antibodies (DSA) post-transplant, time to first biopsy-proven acute rejection episode, freedom from CLAD, graft survival and overall survival.
View Article and Find Full Text PDFCell Host Microbe
January 2025
Department of Pathology and Immunology, Washington University School of Medicine in St. Louis, Saint Louis, MO 63110, USA. Electronic address:
Here, we explore the relationship between dietary fibers, colonic epithelium major histocompatibility complex class II (MHC-II) expression, and immune cell interactions in regulating susceptibility to Clostridioides difficile infection (CDI). We find that a low-fiber diet increases MHC-II expression in the colonic epithelium, which, in turn, worsens CDI by promoting the development of pathogenic CD4 intraepithelial lymphocytes (IELs). The influence of dietary fibers on MHC-II expression is mediated by its metabolic product, acetate, and its receptor, free fatty acid receptor 2 (FFAR2).
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