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The pathogenesis involves a breakdown of self-tolerance, enhanced antigen presentation, T and B lymphocyte activation, autoantibody production, and cytokine-mediated thyroid tissue damage

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its depletion therefore precipitates ferroptosis ( + , prevents copper binding to lipoylated proteins and restrains cuproptosis (64) demonstrated that disulfiramcopper (DSF/Cu) blocks ubiquitin-dependent degradation of the cystine transporter xCT, leading to GSH exhaustion, lipid-peroxide accumulation and compensatory xCT up-regulation

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