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• W2000782751 abstract "Abstract CD4 + T lymphocytes are required to induce spontaneous autoimmune diabetes in the NOD mouse. Since pancreatic β cells upregulate Fas expression upon exposure to pro‐inflammatory cytokines, we studied whether the diabetogenic action of CD4 + T lymphocytes depends on Fas expression on target cells. We assayed the diabetogenic capacity of NOD spleen CD4 + T lymphocytes when adoptively transferred into a NOD mouse model combining: (i) Fas‐deficiency, (ii) FasL‐deficiency, and (iii) SCID mutation. We found that CD4 + T lymphocytes require Fas expression in the recipients' target cells to induce diabetes. IL‐1β has been described as a key cytokine involved in Fas upregulation on mouse β cells. We addressed whether CD4 + T cells require IL‐1β to induce diabetes. We also studied spontaneous diabetes onset in NOD/IL‐1 converting enzyme‐deficient mice, in NOD/IL‐1β‐deficient mice, and CD4 + T‐cell adoptively transferred diabetes into NOD/SCID IL‐1β‐deficient mice. Neither IL‐1β nor IL‐18 are required for either spontaneous or CD4 + T‐cell adoptively transferred diabetes. We conclude that CD4 + T‐cell‐mediated β‐cell damage in autoimmune diabetes depends on Fas expression, but not on IL‐1β unveiling the existing redundancy regarding the cytokines involved in Fas upregulation on NOD β cells in vivo." @default.
• W2000782751 created "2016-06-24" @default.
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• W2000782751 date "2011-04-13" @default.
• W2000782751 modified "2023-10-18" @default.
• W2000782751 title "In vivo diabetogenic action of CD4+ T lymphocytes requires Fas expression and is independent of IL-1 and IL-18" @default.
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• W2000782751 doi "https://doi.org/10.1002/eji.201041216" @default.
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