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Adv."],"published-print":{"date-parts":[[2026,5,29]]},"abstract":"<jats:p>Granuloma annulare (GA) and cutaneous sarcoidosis (cSAR) have an overlapping immunopathology, in which the aberrant activation of macrophages by IFN-\u03b3 constitutes a central driver. Nevertheless, the molecular understanding in GA and cSAR macrophages remains limited. We reanalyzed single-cell RNA sequencing data of GA and cSAR and performed in vitro experiments with primary human cells showing that oxidative phosphorylation (OXPHOS) is a dominant metabolic pathway in IFN-\u03b3\u2013activated macrophages. Furthermore, we identify an IFN-\u03b3\u2013induced response network in GA and cSAR macrophages, sensitive to electron transport chain (ETC) inhibitors. Guanylate-binding protein 1 (GBP1) was central in controlling IFN-\u03b3\u2013mediated macrophage activation. Meanwhile, inhibition of IFN-\u03b3 signaling, ETC complexes, and GBP1 reduced granuloma formation in a human in vitro model. Metformin, a clinically used ETC complex I inhibitor, suppressed IFN-\u03b3 activation of macrophages and in vitro granulomas. 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