IL-21 and IL-21R are not required for development of Th17 cells and autoimmunity in vivo.

Authors: Sonderegger, I  Kisielow, J  Meier, R  King, C  Kopf, M 
Citation: Sonderegger I, etal., Eur J Immunol. 2008 Jul;38(7):1833-8.
Pubmed: (View Article at PubMed) PMID:18546146
DOI: Full-text: DOI:10.1002/eji.200838511

Th17 cells have been recognized as the central effectors in organ-related autoimmune diseases. IL-6 is a key factor that reciprocally regulates Th17 and Foxp3(+) Treg differentiation by inhibition of TGF-beta induced Foxp3 and induction of RORgammat, a Th17 lineage-specific transcription factor. Recently IL-21 has been suggested to induce RORgammat and Th17 development in the absence of IL-6. However, the relevance of IL-21 for Th17-dependent inflammatory responses in vivo remains unclear. In this study, we demonstrate that differentiation of IL-17-producing CD4 T cells, their recruitment to inflamed organs, and the development of autoimmune disease was not affected in il21R(-/-) and il21(-/-) mice in models of myelin oligodendrocyte glycoprotein-induced autoimmune encephalitis and autoimmune myocarditis. IL-6 induced Th17 differentiation independent of and much more potently than IL-21 in vitro. These data suggest that IL-6 is sufficient to drive Th17 development and associated autoimmunity in vivo in the absence of IL-21 or IL-21R.

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CRRD ID: 6892939
Created: 2012-08-17
Species: All species
Last Modified: 2012-08-17
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.