AI Article Synopsis
- IL-22 has a dual role in tumor development, where short-term production protects against stress, but excessive activity can fuel tumor growth, emphasizing the need for its regulation.
- The study finds increased levels of IL-17+IL-22+ cells and TGF-β1 in colorectal cancer tissue, while IL-22-only producing cells remain unchanged.
- TGF-β signaling enhances the emergence of IL-22-producing Th17 cells, promoting tumor growth in mice, and this process involves AhR induction and PI3K signaling pathways.
Article Abstract
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-β1 promotes the differentiation of Th17 cells, which are known to be a major source of IL-22, but the effect of TGF-β 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-β1 in colorectal cancer compared to normal adjacent tissue, whereas the frequency of IL-22 single producing cells is not changed. Accordingly, TGF-β 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-β signaling. We show that TGF-β, via AhR induction, and PI3K signaling promotes IL-22 production in Th17 cells.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7248087 | PMC |
| http://dx.doi.org/10.1038/s41467-020-16363-w | DOI Listing |
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