ArticleArthritis & rheumatology (Hoboken, N.J.)2026
Investigating the Role of Type I Interferon Signaling on Muscle Disease Using Mouse Models.
Article in Arthritis & rheumatology (Hoboken, N.J.), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
objectiveDysregulated type I interferon (IFN) signaling contributes to autoimmune myositis pathogenesis. We investigated the therapeutic effects of JAK inhibitors in two mouse models. We also examined how type I IFNs affect muscle vasculature.
methodsMyositis was induced in major histocompatibility complex class I double transgenic ([TRE-H-2K
resultsTofacitinib-but not baricitinib-significantly reduced IFN scores in mice with severe myositis (P < 0.05). Survival differed across groups (overall log-rank P < 0.01), with untreated- and baricitinib-treated HT mice showing shorter survival than BL/6 controls, whereas tofacitinib-treated mice did not differ from controls. IFNβ overexpression induced muscle inflammation (P < 0.01), reduced grip strength (P < 0.0001), and increased the IFN score (P < 0.0001) and H2Kb (P < 0.0001) expression.
conclusionTofacitinib reduced the IFN signature, and survival in this group did not differ significantly from healthy controls, whereas untreated and baricitinib-treated HT mice showed shorter survival; functional improvement was not observed. Our results also show that type I IFN signaling contributes to muscle inflammation and weakness, making it a key driver of muscle damage and thereby reinforcing its potential as a therapeutic target.
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