The complement system is a crucial part of the innate immune system. In systemic autoimmune disorders, its effects tend to be protective. On the contrary, in the autoimmune thyroid disorders (AIT) the complement actively attacks thyrocytes, which express a number of complement components as well as complement inhibitory molecules. According to the experimental studies different ways of complement activation might occur in the thyroid tissue. All ensue via the classical pathway that is started either by immune complexes containing complement activating autoantibodies against thyroid autoantigens, or by direct binding of C4 to the molecule of thyroid peroxidase (TPO); or by direct complement activation by reactive oxygen radicals. Thyrocytes are relatively resistant to the complement attack. However, sublethaly injured thyrocytes release proinflammatory cytokines and reactive oxygen radicals and thus promote the inflammatory process in the thyroid. So far, the clinical significance of the complement in the thyroid has been studied only in postpartum thyroiditis. The exact role of complement in the pathogenesis of AIT remains to be elucidated.

        Key words: complement autoimmune thyroiditis, thyroid peroxidase, cytokines.