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- W4313368977 abstract "Abstract Th17 cells have been implicated in the pathogenesis of inflammatory bowel diseases. Despite their inflammatory nature, Th17 cells are highly enriched in the intestines under homeostatic conditions. However, it remains unclear as to their exact role during intestinal homeostasis. We found that CBir1 TCR transgenic (CBir1 Tg) mice, which are specific for an immunodominant microbiota antigen CBir1 flagellin, demonstrated a higher levels of Th17 cells and higher amounts of amphiregulin (Areg), which has been recently shown to be highly protective at the mucosal surfaces, in the intestines compared to wild-type (WT) mice. Administration of Areg to WT mice led to decreased intestinal injury and higher level of tight-junction protein expression upon DSS insult. We further showed that Th17 cells produced higher levels of Areg compared to Th1 cells, and Areg inhibited T cell proliferation. Consistently, TCRβ/δ−/− mice transferred with Th17 cells developed less severe colitis compared with mice received Th1 cells. Additionally, TGF-β and IL-6, but not IL-23, the critical cytokines for Th17 development, promoted Areg expression in T cells in a time and dose dependent manner. Treatment with IL-21, but not IL-17, which are Th17 signature cytokines, upregulated Areg. Consistently, IL-21R−/− T cells produced lower levels of Areg. Mechanically, Stat3 mediates Areg expression in T cells, in that IL-6 promoted Stat3 activation, and IL-6 did not induce Areg expression in Stat3−/− T cells. Furthermore, Areg expression was lower in Stat3−/− T cells compared with WT T cells under Th17 polarization conditions. Collectively, these findings reveal that intestinal Th17 cells contribute to intestinal homeostasis and immune regulation by production of Areg." @default.
- W4313368977 created "2023-01-06" @default.
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- W4313368977 date "2020-05-01" @default.
- W4313368977 modified "2023-09-26" @default.
- W4313368977 title "Th17 cell production of amphregulin contributes to the intestinal homeostasis" @default.
- W4313368977 doi "https://doi.org/10.4049/jimmunol.204.supp.158.2" @default.
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