Thyrocyte-interleukin-1 interactions

Autoimmune thyroid disease is the most common organ-specific autoimmune dis ease and is a very common cause of thyroid dysfunction such as autoimmune h ypothyroidism, Graves' disease and postpartum thyroiditis. The thyroid glan d from patients with autoimmune thyroid disease is morphologically characte rized by massive infiltration of lymphoid cells. The interleukin-1 (IL-1) f amily of molecules is together with other cytokines an integral component o f the complex intercellular communication required to mount and control an immune response. IL-1 alpha/beta in moderate and high concentrations reversibly inhibit thyr oid cell function, while IL-1 beta in low concentrations stimulates thyroid cell function. The biphasic, non-cytotoxic and reversible influence of IL- 1 supports a role of IL-1 in the physiological regulation of thyroid cell f unction. IL-1 stimulates the guanylate mediated pathways and inhibits the a denylate cyclase mediated pathways. All IL-1 effects are counteracted by IL -1 receptor antagonist indicating that the effects are exerted through acti vation of specific IL-1 receptors on thyrocytes. Furthermore, IL-1 induces or enhances expression of a number of immunologically active molecules such as adhesion molecules, cytokines, and complement regulatory proteins in th yroid epithelial cells. IL-1 may thus play a role during physiological as w ell as pathophysiological conditions contributing to for example the euthyr oid sick syndrome and development of thyroid autoimmunity. This review summarizes current litterature on the phenomenological in vitro influence of IL-1 on the thyroid cell.