Introduction According to current views on the etiology of autoimmune thyroiditis a modification of the normal antigens of the thyroid is produced and the tolerance of T cells is broken, followed by a co-operation between T and B cells resulting in a humoral or cell mediated immune response (1). One of the main problems in the pathogenesis of chronic thyroiditis is to recognize the event triggering off the breakage of the tolerance. The antigen activity in a complex molecule is related to the interplay of different portions of the molecule with T and B cells (2, 3). Antigens have a carrier function which is recognized by the T cell and a hapten function towards which B cells have a specific receptor and produce an immune response. The appearance in a "self" molecule of a carrier may be the initial event in the breakage of the tolerance and in the production
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G Salabe (1975) studied this question.