How do T cells mediate autoimmune thyroiditis?

Susceptibility to experimental autoimmune thyroiditis (EAT) is linked to the mouse H-2 complex(1). Initiation of the condition by the thyroid antigen, thyroglobulin (Tg), requires T cells from susceptible mice(2). These T cells are autoreactive in that they recognize Tg and proliferate in vitro in response to it(3). The 1980s have brought forth confirmatory data from several laboratories on T-cell autoreactivity to mouse Tg both in vivo(4,5) and in vitro(6-13), and its correlation with EAT susceptibility. T cells from patients with Hashimoto's thyroiditis (HT), may proliferate in response to stimulation in vitro with human Tg(14-16). The capacity of murine T cells to expand and differentiate in vitro(17,18) and to serve as effector cells causing thyroiditis in vivo(7,8, 11,12) is strongly indicative of their pathogenic role. We are now in a position to discuss not only if T cells mediate autoimmune thyroiditis, but how they might contribute to the pathogenic process. At least two antigen-activated T-cell subsets seem to participate in initiating and perpetuating thyroid destruction. In this article, Yi-chi Kong and her colleagues present a synopsis of the supporting data from the mouse model and parallel findings from HT patients.