Abstract
The article presents current evidence on molecular mimicry between Yersinia enterocolitica antigens and thyroid
structures, particularly the thyrotropin receptor and thyroid peroxidase. Cross-reactive immune responses are shown to promote
both humoral and cellular immunity, including activation of Th1 and Th17 pathways, impairment of regulatory T-cell function,
and excessive autoantibody production.
Special attention is given to the systemic consequences of thyroid dysfunction, particularly its effects on the cardiovascular
system. Altered thyroid hormone levels trigger electrophysiological remodeling of the myocardium by modulating ion channels,
β-adrenergic sensitivity, and repolarization. These changes create a substrate for a wide spectrum of cardiac arrhythmias,
ranging from sinus bradycardia and conduction disturbances in hypothyroidism to tachyarrhythmias, including atrial fibrillation,
in thyrotoxic states.
In addition, the role of immune-inflammatory mechanisms in the development of so-called autoimmune channelopathies is
discussed because these processes can directly affect the electrophysiological properties of cardiomyocytes.
Thus, molecular mimicry between Yersinia enterocolitica and thyroid antigens is a key pathogenic mechanism linking infectious
triggers to autoimmune thyroiditis and its cardiovascular complications. A unified pathophysiological continuum «infection–
autoimmunity–thyroid dysfunction–cardiac disorders» emerges, underscoring the need for a multidisciplinary approach to the
diagnosis and management of affected patients.
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