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Enhanced iodide intake in NOD.H2(h4) mice accelerates the incidence and severity of spontaneous autoimmune thyroiditis (SAT) via an unknown mechanism. A plausible hypothesis is that iodide-induced apoptosis of thyrocytes can create imbalances in antigenic load and/or disruption of immunoregulatory mechanisms that facilitate activation of autoreactive T cells in cervical lymph nodes draining the thyroid.

Apoptosis of NOD.H2h4Thyrocytes by Low Concentrations of Iodide is Associated with Impaired Control of Oxidative Stress

Apoptosis of NOD.H2^h4Thyrocytes by Low Concentrations of Iodide is Associated with Impaired Control of Oxidative Stress