ArticleAnimal models and experimental medicine2026
GS-9620 alleviates psoriasis-like inflammation by regulating autophagy in keratinocytes.
Article in Animal models and experimental medicine, 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
backgroundPsoriasis is an immune-driven dermatosis marked by keratinocyte hyperproliferation. GS-9620, a TLR7 agonist, previously mitigated EV71-triggered inflammation in mice; here we probe its anti-psoriatic potential and mechanisms.
methodsIMQ-induced psoriasis-like mice were treated with GS-9620 or MTX; severity was tracked by PASI and histology. Skin/spleen cytokines (IL-1β, IL-6, IL-18, HMGB1, TNF-α) were quantified via ELISA; immune subsets were quantified by flow cytometry. Autophagy proteins (ATG5/12/16 L1) and NLRP3 were assessed by IHC/Western blot. In vitro, M5-stimulated primary keratinocytes were treated with GS-9620 ± autophagy modulators, followed by cytokine and protein analyses.
resultsGS-9620 markedly reduced erythema, scaling and epidermal thickness, lowered skin and systemic cytokines, and decreased splenic CD3
conclusionsGS-9620 alleviates psoriasis by enhancing autophagy and dampening NLRP3-mediated inflammation, offering a promising therapeutic avenue.
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