| First Author | Okamoto M | Year | 2009 |
| Journal | Nat Immunol | Volume | 10 |
| Issue | 8 | Pages | 872-9 |
| PubMed ID | 19561615 | Mgi Jnum | J:151652 |
| Mgi Id | MGI:4354692 | Doi | 10.1038/ni.1747 |
| Citation | Okamoto M, et al. (2009) Mina, an Il4 repressor, controls T helper type 2 bias. Nat Immunol 10(8):872-9 |
| abstractText | T helper type 2 (T(H)2) bias, which is the propensity of naive CD4(+) T cells to differentiate into interleukin 4 (IL-4)-secreting T(H)2 cells, is a genetic trait that affects susceptibility to infectious, autoimmune and allergic diseases. T(H)2 bias correlates with the amount of IL-4 initially secreted by newly activated helper T cells that feeds back positively through the pathway of the IL-4 receptor and the transcription factors STAT6 and GATA-3 to drive T(H)2 development. Here we identify Mina, a member of the jumonji C (JmjC) protein family, as a genetic determinant of T(H)2 bias. Mina specifically bound to and repressed the Il4 promoter. Mina overexpression in transgenic mice impaired Il4 expression, whereas its knockdown in primary CD4(+) T cells led to Il4 derepression. Our findings collectively provide mechanistic insight into an Il4-regulatory pathway that controls helper T cell differentiation and genetic variation in T(H)2 bias. |
