{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Shen Y"],"funding":["National Natural Science Foundation of China","National Natural Science Foundation of China (National Science Foundation of China)"],"pagination":["2924"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6606754"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["10(1)"],"pubmed_abstract":["Fas induces apoptosis in activated T cell to maintain immune homeostasis, but the effects of non-apoptotic Fas signaling on T cells remain unclear. Here we show that Fas promotes T<sub>H</sub>9 cell differentiation by activating NF-κB via Ca<sup>2+</sup>-dependent PKC-β activation. In addition, PKC-β also phosphorylates p38 to inactivate NFAT1 and reduce NFAT1-NF-κB synergy to promote the Fas<sup>-</sup>induced T<sub>H</sub>9 transcription program. Fas ligation exacerbates inflammatory bowel disease by increasing T<sub>H</sub>9 cell differentiation, and promotes antitumor activity in p38 inhibitor-treated T<sub>H</sub>9 cells. Furthermore, low-dose p38 inhibitor suppresses tumor growth without inducing systemic adverse effects. In patients with tumor, relatively high T<sub>H</sub>9 cell nu"],"journal":["Nature communications"],"pubmed_title":["Fas signaling-mediated T<sub>H</sub>9 cell differentiation favors bowel inflammation and antitumor functions."],"pmcid":["PMC6606754"],"funding_grant_id":["31670877"],"pubmed_authors":["Zhang G","Duan M","Lu X","Lu C","Ma Z","Yang D","Wang J","Li X","Guo J","Apetoh L","Cai Z","Miao Y","Chen Y","Shen Y","Zhang B","Song Z"],"additional_accession":[]},"is_claimable":false,"name":"Fas signaling-mediated T<sub>H</sub>9 cell differentiation favors bowel inflammation and antitumor functions.","description":"Fas induces apoptosis in activated T cell to maintain immune homeostasis, but the effects of non-apoptotic Fas signaling on T cells remain unclear. Here we show that Fas promotes T<sub>H</sub>9 cell differentiation by activating NF-κB via Ca<sup>2+</sup>-dependent PKC-β activation. In addition, PKC-β also phosphorylates p38 to inactivate NFAT1 and reduce NFAT1-NF-κB synergy to promote the Fas<sup>-</sup>induced T<sub>H</sub>9 transcription program. Fas ligation exacerbates inflammatory bowel disease by increasing T<sub>H</sub>9 cell differentiation, and promotes antitumor activity in p38 inhibitor-treated T<sub>H</sub>9 cells. Furthermore, low-dose p38 inhibitor suppresses tumor growth without inducing systemic adverse effects. In patients with tumor, relatively high T<sub>H</sub>9 cell nu","dates":{"release":"2019-01-01T00:00:00Z","publication":"2019 Jul","modification":"2026-05-06T22:50:19.57Z","creation":"2019-07-25T07:03:00Z"},"accession":"S-EPMC6606754","cross_references":{"pubmed":["31266950"],"doi":["10.1038/s41467-019-10889-4"]}}