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In vivo diabetogenic action of CD41+ T lymphocytes requires Fas expression and is independent of IL-1 and IL-18

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Issue date
2011
Author
Wen, Li
Green, E. Allison
Stratmann, Thomas
Panosa, Anaïs
Gomis, Ramon
Eynon, Elizabeth E.
Flavell, Richard A.
Mezquita, Jovita A.
Mora Giral, Concepció
Suggested citation
Wen, Li; Green, E. Allison; Stratmann, Thomas; Panosa, Anaïs; Gomis, Ramon; Eynon, Elizabeth E.; ... Mora Giral, Concepció. (2011) . In vivo diabetogenic action of CD41+ T lymphocytes requires Fas expression and is independent of IL-1 and IL-18. European Journal of Immunology, 2011, vol. 41, núm. 5, p. 1344-51. https://doi.org/10.1002/eji.201041216.
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Abstract
CD4+ T lymphocytes are required to induce spontaneous autoimmune diabetes in the NOD (Non Obese Diabetic) mouse. Since pancreatic β cells upregulate Fas expression upon exposure to proinflammatory 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: a) Fas-deficiency, b) FasL-deficiency, and c) the 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 up-regulation on mouse β cells. We addressed whether CD4+ T cells require IL-1β to induce diabetes. We also studied spontaneous diabetes onset in NOD/ICE (Interleukin-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.
URI
http://hdl.handle.net/10459.1/71127
DOI
https://doi.org/10.1002/eji.201041216
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European Journal of Immunology, 2011, vol. 41, núm. 5, p. 1344-51
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