| First Author | Sonderegger I | Year | 2008 |
| Journal | Eur J Immunol | Volume | 38 |
| Issue | 7 | Pages | 1833-8 |
| PubMed ID | 18546146 | Mgi Jnum | J:137377 |
| Mgi Id | MGI:3799407 | Doi | 10.1002/eji.200838511 |
| Citation | Sonderegger I, et al. (2008) IL-21 and IL-21R are not required for development of Th17 cells and autoimmunity in vivo. Eur J Immunol 38(7):1833-8 |
| abstractText | 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.See accompanying Commentary http:dx.doi.org/10.1002/eji.200838529Supporting information for this article is available at http://www.wiley-vch.de/contents/jc_2040/2008/38511_s.pdf. |
