| First Author | Park S | Year | 2017 |
| Journal | Nat Commun | Volume | 8 |
| Pages | 16037 | PubMed ID | 28855737 |
| Mgi Jnum | J:246060 | Mgi Id | MGI:5920904 |
| Doi | 10.1038/ncomms16037 | Citation | Park S, et al. (2017) Capicua deficiency induces autoimmunity and promotes follicular helper T cell differentiation via derepression of ETV5. Nat Commun 8:16037 |
| abstractText | High-affinity antibody production through the germinal centre (GC) response is a pivotal process in adaptive immunity. Abnormal development of follicular helper T (TFH) cells can induce the GC response to self-antigens, subsequently leading to autoimmunity. Here we show the transcriptional repressor Capicua/CIC maintains peripheral immune tolerance by suppressing aberrant activation of adaptive immunity. CIC deficiency induces excessive development of TFH cells and GC responses in a T-cell-intrinsic manner. ETV5 expression is derepressed in Cic null TFH cells and knockdown of Etv5 suppresses the enhanced TFH cell differentiation in Cic-deficient CD4+ T cells, suggesting that Etv5 is a critical CIC target gene in TFH cell differentiation. Furthermore, we identify Maf as a downstream target of the CIC-ETV5 axis in this process. These data demonstrate that CIC maintains T-cell homeostasis and negatively regulates TFH cell development and autoimmunity. |
