| First Author | Kim HS | Year | 2017 |
| Journal | J Exp Med | Volume | 214 |
| Issue | 11 | Pages | 3381-3398 |
| PubMed ID | 29018045 | Mgi Jnum | J:251492 |
| Mgi Id | MGI:5924753 | Doi | 10.1084/jem.20170523 |
| Citation | Kim HS, et al. (2017) PTEN drives Th17 cell differentiation by preventing IL-2 production. J Exp Med 214(11):3381-3398 |
| abstractText | T helper 17 (Th17) cells are a CD4(+) T cell subset that produces IL-17A to mediate inflammation and autoimmunity. IL-2 inhibits Th17 cell differentiation. However, the mechanism by which IL-2 is suppressed during Th17 cell differentiation remains unclear. Here, we show that phosphatase and tensin homologue (PTEN) is a key factor that regulates Th17 cell differentiation by suppressing IL-2 production. Th17-specific Pten deletion (Pten(fl/fl)Il17a(cre) ) impairs Th17 cell differentiation in vitro and ameliorated symptoms of experimental autoimmune encephalomyelitis (EAE), a model of Th17-mediated autoimmune disease. Mechanistically, Pten deficiency up-regulates IL-2 and phosphorylation of STAT5, but reduces STAT3 phosphorylation, thereby inhibiting Th17 cell differentiation. PTEN inhibitors block Th17 cell differentiation in vitro and in the EAE model. Thus, PTEN plays a key role in Th17 cell differentiation by blocking IL-2 expression. |
