{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Zhang ZD"],"funding":["National Natural Science Foundation of China","National Natural Science Foundation of China (National Science Foundation of China)"],"pagination":["275-291"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10901794"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["21(3)"],"pubmed_abstract":["STING (also known as MITA) is an adaptor protein that mediates cytoplasmic DNA-triggered signaling, and aberrant activation of STING/MITA by cytosolic self-DNA or gain-of-function mutations causes severe inflammation. Here, we show that STING-mediated inflammation and autoimmunity are promoted by RNF115 and alleviated by the RNF115 inhibitor disulfiram (DSF). Knockout of RNF115 or treatment with DSF significantly inhibit systemic inflammation and autoimmune lethality and restore immune cell development in Trex1<sup>-/-</sup> mice and STING<sup>N153S/WT</sup> bone marrow chimeric mice. In addition, knockdown or pharmacological inhibition of RNF115 substantially downregulate the expression of IFN-α, IFN-γ and proinflammatory cytokines in PBMCs from patients with systemic lupus erythematosus "],"journal":["Cellular & molecular immunology"],"pubmed_title":["Disulfiram ameliorates STING/MITA-dependent inflammation and autoimmunity by targeting RNF115."],"pmcid":["PMC10901794"],"funding_grant_id":["31930040","823B1006"],"pubmed_authors":["Zhong B","Xiong TC","Chen M","Lin YL","Li FX","Gan H","Zhang ZD","Wei Y","Zhang Q","Lin D","Shi CR","Shuai X","Chen X"],"additional_accession":[]},"is_claimable":false,"name":"Disulfiram ameliorates STING/MITA-dependent inflammation and autoimmunity by targeting RNF115.","description":"STING (also known as MITA) is an adaptor protein that mediates cytoplasmic DNA-triggered signaling, and aberrant activation of STING/MITA by cytosolic self-DNA or gain-of-function mutations causes severe inflammation. Here, we show that STING-mediated inflammation and autoimmunity are promoted by RNF115 and alleviated by the RNF115 inhibitor disulfiram (DSF). Knockout of RNF115 or treatment with DSF significantly inhibit systemic inflammation and autoimmune lethality and restore immune cell development in Trex1<sup>-/-</sup> mice and STING<sup>N153S/WT</sup> bone marrow chimeric mice. In addition, knockdown or pharmacological inhibition of RNF115 substantially downregulate the expression of IFN-α, IFN-γ and proinflammatory cytokines in PBMCs from patients with systemic lupus erythematosus ","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Mar","modification":"2025-04-03T23:36:04.976Z","creation":"2025-04-03T23:36:04.976Z"},"accession":"S-EPMC10901794","cross_references":{"pubmed":["38267694"],"doi":["10.1038/s41423-024-01131-3"]}}