Abstract
Efficient antigen presentation requires the provision of a costimulatory signal, the best characterized of which is B7/BB1. It is unclear whether thyroid cells expressing class II molecules can present autoantigens to T cells, although this has been suggested as an important mechanism in the initiation of Graves' disease and Hashimoto's thyroiditis. We have found that thyroid cells from patients with thyroid autoimmunity do not express B7/BB1 in vivo or in vitro, even after activation with the cytokines interleukin-1 or gamma-interferon, or with a phorbol ester. Increased numbers of CD20+ B cells and CD14+ dendritic cells expressing B7/BB1 were found in intrathyroidal lymphocyte preparations from such patients compared to peripheral blood. These results suggest that conventional antigen-presenting cells rather than thyroid cells provide B7/BB1 costimulatory activity in autoimmune thyroid disease, and argue against a role for the thyroid cells themselves in autoantigen presentation to T cells via the B7/BB1 pathway.
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