Abstract

A characteristic immunopathologic feature of human autoimmune thyroid disease (ATD) is the ectopic expression of HLA class II antigens by a proportion of the thyroid follicular cells (TFC) in the affected gland [1]. This finding prompted the notion that this expression might be the primary aberration which would enable TFC to present specific self constituents to potentially autoreactive T lymphocytes in the “appropriate” context, and thus initiate the autoimmune response leading to chronic inflammation and parenchymal damage [2]. In support of their putative role as antigen-presenting cells, HLA-DR positive TFC cultured from ATD tissues have been shown to present virally-encoded [3] and autologous thyroid [4] antigens to specific T cell clones in vitro.

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