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This study aimed to identify drugs that can inhibit both IFN\u2010I and autoantibody production.<\/jats:p>\n <\/jats:sec>\n \n Methods<\/jats:title>\n We identified an inhibitor of IFN\u2010I production from a chemical library. Subsequently, we examined its efficacy and underlying mechanisms in suppressing the expression and phosphorylation of upstream signaling molecules for IFN\u2010I production and the differentiation of B cells into plasma cells. Additionally, we examined whether it could alleviate disease severity in SLE\u2010prone mice.<\/jats:p>\n <\/jats:sec>\n \n Results<\/jats:title>\n We showed that vorinostat, a clinically approved pan\u2010histone deacetylase (HDAC) inhibitor, inhibited both IFN\u2010I production and plasma cell differentiation. Vorinostat suppressed IFN\u2010I production by inhibiting TBK1 phosphorylation and the subsequent IRF3 nuclear translocation and suppressed plasma cell differentiation by inhibiting the expression of essential transcriptional factors for plasma cells. Notably, inhibiting HDAC6 suppressed IFN\u2010I induction and plasma cell differentiation. Furthermore, vorinostat ameliorated lung inflammation in STING\u2010associated vasculopathy with onset in infancy mice by decreasing IFN\u2010I and alleviated the mortality and severity of renal disease in New Zealand Black\/White F1 mice by suppressing IFN\u2010I induction and B cell differentiation.<\/jats:p>\n <\/jats:sec>\n \n Conclusion<\/jats:title>\n Vorinostat ameliorates the severity of disease in SLE\u2010prone mice by simultaneously suppressing IFN\u2010I production and plasma cell differentiation by targeting HDAC6. Thus, vorinostat is a promising therapeutic agent for SLE and may benefit patients with SLE requiring more effective and better\u2010tolerated therapies.<\/jats:p>\n \n \n \n image<\/jats:alt-text>\n <\/jats:graphic>\n <\/jats:boxed-text>\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1002\/art.43434","type":"journal-article","created":{"date-parts":[[2025,11,14]],"date-time":"2025-11-14T12:58:45Z","timestamp":1763125125000},"page":"880-895","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Identification of Histone Deacetylase Inhibitor Targeting Type I Interferon and B Cell Abnormalities in Systemic Lupus Erythematosus"],"prefix":"10.1002","volume":"78","author":[{"given":"Takehiro","family":"Hirayama","sequence":"first","affiliation":[{"name":"Department of Respiratory Medicine and Clinical Immunology, Graduate School of Medicine Osaka University Osaka Japan"},{"name":"Department of Immunopathology, Immunology Frontier 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