Abstract

Over the last decade it has become evident that thyroid follicular cells express a number of immunologically active molecules in autoimmune thyroid disease that may endow them with the capacity to interact with cells of the classical immune system. Expression of major histocompatibility complex class II molecules is induced by gamma-interferon, but there is no evidence yet that thyroid follicular cells can concurrently express the costimulatory signals necessary for class II expression to result in T cell stimulation: in this situation, class II expression may have a protective role, inducing T cell anergy. Thyroid follicular cells also express a variety of cell surface proteins (in particular CD59) that may protect the cells from complement attack. On the other hand, the expression of adhesion molecules and cytokines by thyrocytes would seem to be harmful, as these are likely to exacerbate autoimmune injury. Further study of the immunological role of thyroid follicular cells will shed new light on the pathogenesis of Graves' disease and autoimmune hypothyroidism, and may lead to novel therapeutic approaches to these disorders.

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