First Author | Schmitt N | Year | 2014 |
Journal | Nat Immunol | Volume | 15 |
Issue | 9 | Pages | 856-65 |
PubMed ID | 25064073 | Mgi Jnum | J:260275 |
Mgi Id | MGI:6140280 | Doi | 10.1038/ni.2947 |
Citation | Schmitt N, et al. (2014) The cytokine TGF-beta co-opts signaling via STAT3-STAT4 to promote the differentiation of human TFH cells. Nat Immunol 15(9):856-65 |
abstractText | Understanding the developmental mechanisms of follicular helper T cells (TFH cells) in humans is relevant to the clinic. However, the factors that drive the differentiation of human CD4+ helper T cells into TFH cells remain largely undefined. Here we found that transforming growth factor-beta (TGF-beta) provided critical additional signals for the transcription factors STAT3 and STAT4 to promote initial TFH differentiation in humans. This mechanism did not appear to be shared by mouse helper T cells. Developing human TFH cells that expressed the transcriptional repressor Bcl-6 also expressed RORgammat, a transcription factor typically expressed by the TH17 subset of helper T cells. Our study documents a mechanism by which TFH cells and TH17 cells emerge together in inflammatory environments in humans, as is often observed in many human autoimmune diseases. |