IL-22 is expressed by Th17 cells in an IL-23-dependent fashion, but not required for the development of autoimmune encephalomyelitis

Katharina Kreymborg, Ruth Etzensperger, Laure Dumoutier, Stefan Haak, Angelita Rebollo, Thorsten Buch, Frank L. Heppner, Jean Christophe Renauld, Burkhard Becher

Research output: Contribution to journalArticlepeer-review

278 Scopus citations

Abstract

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.

Original languageEnglish
Pages (from-to)8098-8104
Number of pages7
JournalJournal of Immunology
Volume179
Issue number12
DOIs
StatePublished - 15 Dec 2007
Externally publishedYes

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