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Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes
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Published on: September 26, 2013

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PTEN drives Th17 cell differentiation by preventing IL-2 production

Hyeong Su Kim1, Sung Woong Jang1, Wonyong Lee1

  • 1Department of Life Science, Sogang University, Seoul, South Korea.

The Journal of Experimental Medicine
|October 12, 2017
PubMed

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 ) 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.

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