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10.1186/s12964-025-02575-4 http://scihub22266oqcxt.onion/10.1186/s12964-025-02575-4 41366425!?!41366425 Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=41366425&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215       Cell+Commun+Signal 2025 ; ? (?): ? Nephropedia Template TP {{tp|p=41366425|t=2025. IL-1beta-mediated suppression of CIITA attenuates IFN-gamma-induced MHC-II expression on Fibroblasts |pdf=|usr=}}{{41366425}} gab.com Text IL-1beta-mediated suppression of CIITA attenuates IFN-gamma-induced MHC-II expression on Fibroblasts JO: Cell Commun Signal http://www.kidney.de/pget.php?&tw=1&pmid=41366425 #FOAvip BACKGROUND: Cancer-associated fibroblasts (CAFs) are key regulators in tumor microenvironment and tumor immunity, partly through MHC-II expression that modulates T-cell differentiation. However, the upstream cytokine signals controlling MHC-II expression in fibroblasts still remain poorly defined. METHODS: We examined MHC-II expression on fibroblasts under stimulation with interferon-gamma (IFN-gamma) and interleukin-1beta (IL-1beta) by using flow cytometry, transcriptomic analysis, and qRT-PCR. To dissect transcriptional regulation, we generated CIITA-overexpressing and CIITA-deficient fibroblast lines by lentiviral transduction and CRISPR/Cas9-mediated editing. Public scRNA-seq, ATAC-seq, and ChIP-seq datasets were further analyzed to validate molecular mechanisms. RESULTS: IFN-gamma robustly up-regulated MHC-II expression on fibroblasts, while IL-1beta selectively suppressed this induction without affecting PD-L1. Mechanistically, IL-1beta attenuated IFN-gamma-induced CIITA expression at the mRNA level but did not alter STAT1 abundance or phosphorylation. Functional assays confirmed that CIITA was indispensable for IFN-gamma-driven MHC-II expression in fibroblasts. Integration of transcriptomic and epigenomic data demonstrated that CIITA directly bound MHC-II gene promoters and regulated chromatin accessibility. CONCLUSIONS: Our study identifies an IFN-gamma/STAT1/CIITA axis as the central regulator of MHC-II expression in fibroblasts and reveals IL-1beta as a potent suppressor of this pathway. These findings highlight a novel cytokine-mediated regulatory mechanism underlying CAF-driven immunosuppression within the tumor microenvironment. Twit Text FOAVip IL-1beta-mediated suppression of CIITA attenuates IFN-gamma-induced MHC-II expression on Fibroblasts ????Cell Commun Signal http://www.kidney.de/pget.php?&tw=1&pmid=41366425 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=41366425 #FOAvip English Wikipedia <ref>{{Cite pmid|41366425}}</ref> IL-1beta-mediated suppression of CIITA attenuates IFN-gamma-induced MHC-II expression on Fibroblasts #MMPMID41366425 Chen L; Jiang H; Tan B; Geng R; Chen J; Wu S; Fang Z; Lang Y; Ma H; Zheng X; Jiang J Cell Commun Signal 2025[Dec]; ? (?): ? PMID41366425show ga BACKGROUND: Cancer-associated fibroblasts (CAFs) are key regulators in tumor microenvironment and tumor immunity, partly through MHC-II expression that modulates T-cell differentiation. However, the upstream cytokine signals controlling MHC-II expression in fibroblasts still remain poorly defined. METHODS: We examined MHC-II expression on fibroblasts under stimulation with interferon-gamma (IFN-gamma) and interleukin-1beta (IL-1beta) by using flow cytometry, transcriptomic analysis, and qRT-PCR. To dissect transcriptional regulation, we generated CIITA-overexpressing and CIITA-deficient fibroblast lines by lentiviral transduction and CRISPR/Cas9-mediated editing. Public scRNA-seq, ATAC-seq, and ChIP-seq datasets were further analyzed to validate molecular mechanisms. RESULTS: IFN-gamma robustly up-regulated MHC-II expression on fibroblasts, while IL-1beta selectively suppressed this induction without affecting PD-L1. Mechanistically, IL-1beta attenuated IFN-gamma-induced CIITA expression at the mRNA level but did not alter STAT1 abundance or phosphorylation. Functional assays confirmed that CIITA was indispensable for IFN-gamma-driven MHC-II expression in fibroblasts. Integration of transcriptomic and epigenomic data demonstrated that CIITA directly bound MHC-II gene promoters and regulated chromatin accessibility. CONCLUSIONS: Our study identifies an IFN-gamma/STAT1/CIITA axis as the central regulator of MHC-II expression in fibroblasts and reveals IL-1beta as a potent suppressor of this pathway. These findings highlight a novel cytokine-mediated regulatory mechanism underlying CAF-driven immunosuppression within the tumor microenvironment. ?IL-1beta-mediated suppression of CIITA attenuates IFN-gamma-induced MH(epmc).pdf DeepDyve Pubget Overpricing