NGO ameliorates psoriasis by modulating mitochondrial function and suppressing pSTAT3–IL-17–expressing CD8+ TRM cells

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Abstract Psoriasis is a chronic autoimmune skin disorder characterized by keratinocyte hyperproliferation, persistent inflammation, and frequent relapse. Tissue-resident memory T (TRM) cells, particularly IL-17– and phosphorylated STAT3 (pSTAT3)–expressing CD8+ subsets, have been established as central drivers of disease persistence and recurrence. These pathogenic TRM cells maintain local inflammatory circuits that are poorly targeted by current therapies, which helps to explain the limited durability of clinical remission in many patients. Therefore, strategies for selective suppression of these immune subsets are urgently needed. In this study, we investigated the therapeutic potential of nano-sized graphene oxide (NGO), a biocompatible material with emerging anti-inflammatory properties. NGO treatment significantly enhanced mitochondrial function in immune cells, reflected by improved oxygen consumption rate and reduced mitochondrial reactive oxygen species production. Restoration of mitochondrial homeostasis led to robust suppression of pSTAT3 and IL-17 signaling pathways. Importantly, NGO induced a dose-dependent reduction in the numbers of pathogenic CD8+ TRM17 cells in both murine models of psoriasis and human-patient-derived immune cells. Beyond its direct effects on pathogenic TRM cells, NGO treatment alleviated epidermal hyperplasia and inflammatory infiltration in psoriatic lesions and promoted the expansion of regulatory T cells, thereby fostering an immune environment more conducive to tissue resolution. Taken together, these findings show that NGO exerted potent therapeutic effects by coupling mitochondrial reprogramming with immune modulation. By attenuating pSTAT3–IL-17–driven TRM cell responses and enhancing regulatory T cell activity, NGO has emerged as a promising candidate for durable immunometabolic therapy in psoriasis. Graphical abstract

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