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      Regulation of MHC class I expression by inflammatory cytokines in rat mesangial cells.

      Nephron. Physiology
      Animals, Cells, Cultured, Cytokines, pharmacology, Dose-Response Relationship, Drug, Enzyme Inhibitors, Enzyme-Linked Immunosorbent Assay, Flow Cytometry, Fluorescent Antibody Technique, Glomerular Mesangium, cytology, Histocompatibility Antigens Class II, biosynthesis, metabolism, Humans, Interferon-gamma, Interleukin-1, Male, Molsidomine, analogs & derivatives, Nitric Oxide, Rats, Rats, Sprague-Dawley, Tumor Necrosis Factor-alpha

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          Abstract

          We investigated the regulation of major histocompatibility complex (MHC) class I expression by inflammatory cytokines and nitric oxide (NO) in rat mesangial cells by enzyme-linked immunosorbent assay and flow cytometry. MHC class I molecule expression on mesangial cells was significantly stimulated by interferon gamma, tumor necrosis factor alpha and interleukin 1beta, but not by interleukin 6, in a dose-dependent manner. Addition of SIN-1, an NO donor, did not affect the expression of cytokine-induced MHC class I expression. These results suggest that under inflammatory conditions mesangial cells may act as antigen-presenting cells in response to stimulation by cytokines and may be involved in the pathogenesis of immune-mediated glomerular disease.

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