| First Author | Perez LG | Year | 2020 |
| Journal | Nat Commun | Volume | 11 |
| Issue | 1 | Pages | 2608 |
| PubMed ID | 32451418 | Mgi Jnum | J:292263 |
| Mgi Id | MGI:6447700 | Doi | 10.1038/s41467-020-16363-w |
| Citation | Perez LG, et al. (2020) TGF-beta signaling in Th17 cells promotes IL-22 production and colitis-associated colon cancer. Nat Commun 11(1):2608 |
| abstractText | IL-22 has dual functions during tumorigenesis. Short term IL-22 production protects against genotoxic stress, whereas uncontrolled IL-22 activity promotes tumor growth; therefore, tight regulation of IL-22 is essential. TGF-beta1 promotes the differentiation of Th17 cells, which are known to be a major source of IL-22, but the effect of TGF-beta signaling on the production of IL-22 in CD4+ T cells is controversial. Here we show an increased presence of IL-17+IL-22+ cells and TGF-beta1 in colorectal cancer compared to normal adjacent tissue, whereas the frequency of IL-22 single producing cells is not changed. Accordingly, TGF-beta signaling in CD4+ T cells (specifically Th17 cells) promotes the emergence of IL-22-producing Th17 cells and thereby tumorigenesis in mice. IL-22 single producing T cells, however, are not dependent on TGF-beta signaling. We show that TGF-beta, via AhR induction, and PI3K signaling promotes IL-22 production in Th17 cells. |
