{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,12]],"date-time":"2026-11-12T02:14:28Z","timestamp":1794449668965,"version":"4.9.1"},"reference-count":208,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,3,30]],"date-time":"2026-03-30T00:00:00Z","timestamp":1774828800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:p>Ferroptosis, fundamentally defined as an iron-catalyzed and lipid peroxidation-driven cell death process, constitutes an underlying disease mechanism in autoimmune pathogenesis. Recent studies demonstrate that ferroptosis not only shapes innate and adaptive immune responses-including T and B lymphocytes, macrophages, neutrophils, and dendritic cells-but also remodels inflammatory microenvironments to either preserve tissue integrity or exacerbate damage. Pharmacological modulation of ferroptosis, via iron chelators, GPX4 activation, and lipid peroxidation blockade, hold promise as adjuncts to current immunomodulatory approaches. 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