IL-22 is expressed by TH17 cells in an IL-23-dependent fashion, but not required for the development of autoimmune encephalomyelitis
(2007) Journal of Immunology — Vol. 179, n° 12, p. 8098-8104 (2007)
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- Lately, IL-17-secreting Th cells have received an overwhelming amount of attention and are now widely held to be the major pathogenic population in autoimmune diseases. In particular, IL-22-secreting. Th17 cells were shown to specifically mark the highly pathogenic population of self-reactive T cells in experimental autoimmune encephalomyelitis (EAE). As IL-17A itself was found to only play a minor role during the development of EAE, IL-22 is now postulated to contribute to the pathogenic function of Th17 cells. The goal of this study was to determine the role and function of IL-22 during the development of CNS autoimmunity in vivo. We found that CNS-invading encephalitogenic Th17 cells coexpress IL-22 and that IL-22 is specifically induced by IL-23 in autoimmune-pathogenic CD4(+) T cells in a time- and dose-dependent manner. We next generated IL-22(-/-) mice, which-in contrast to the prediction that expression of inflammatory cytokines by CNS-invading T cells inevitably confers pathogenic function-turned out to be fully susceptible to EAE. Taken together, we show that self-reactive Th cells coexpress IL-17 and IL-22, but that the latter also does not appear to be directly involved in autoimmune pathogenesis of the CNS.
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Kreymborg, K., Etzensperger, R., Dumoutier, L., Haak, S., Rebollo, A., Buch, T., Heppner, F. L., Renauld, J.-C., & Becher, B. (2007). IL-22 is expressed by TH17 cells in an IL-23-dependent fashion, but not required for the development of autoimmune encephalomyelitis. Journal of Immunology, 179(12), 8098-8104. https://doi.org/10.4049/jimmunol.179.12.8098 (Original work published 2007)