| First Author | Dwivedi VP | Year | 2012 |
| Journal | J Biol Chem | Volume | 287 |
| Issue | 5 | Pages | 2943-7 |
| PubMed ID | 22170065 | Mgi Jnum | J:181510 |
| Mgi Id | MGI:5311534 | Doi | 10.1074/jbc.C111.327627 |
| Citation | Dwivedi VP, et al. (2012) Transforming growth factor-beta protein inversely regulates in vivo differentiation of interleukin-17 (IL-17)-producing CD4+ and CD8+ T cells. J Biol Chem 287(5):2943-7 |
| abstractText | TGF-beta is a pleiotropic cytokine that predominantly exerts inhibitory functions in the immune system. Unexpectedly, the in vitro differentiation of both Th17 and Tc17 cells requires TGF-beta. However, animals that are impaired in TGF-beta signaling (TGF-betaRIIDN mice) display multiorgan autoimmune disorders. Here we show that CD4(+) T cells from TGF-betaRIIDN mice are resistant to Th17 cell differentiation and, paradoxically, that CD8(+) T cells from these animals spontaneously acquire an IL-17-producing phenotype. Neutralization of IL-17 or depletion of CD8(+) T cells dramatically inhibited inflammation in TGF-betaRIIDN mice. Therefore, the absence of TGF-beta triggers spontaneous differentiation of IL-17-producing CD8(+) T cells, suggesting that the in vivo and in vitro conditions that promote the differentiation of IL-17-producing CD8(+) T cells are distinct. |
