Passive transfer of experimental allergic thyriditis, delayed hypersensitivity to thyroglobulin and anti-thyroglobulin antibody formation in inbred Lewis rats.

Inbred Lewis rats regularly develop experimental allergic thyroiditis, delayed skin hypersensitivity and Arthus reactivity, and produce anti-thyroglobulin antibodies 14–21 days after immunization with bovine thyroglobulin in adjuvant. Attempts have been made to transfer thyroiditis to normal rats by means of thymus, spleen or lymph node cells, as well as by serum containing anti-thyroid antibodies. The following types of lymphoid cells were used: viable or non-viable cells from donors immunized with bovine thyroglobulin in adjuvant, cells from donors sensitized only with adjuvant, cells from donors immunized with adjuvant alone and mixed with thyroglobulin prior to the injection into recipients, and cells from donors injected with egg albumin in adjuvant. Thyroglobulin-sensitive lymph node cells were most effective in transferring thyroiditis, delayed skin hypersensitivity and anti-thyroglobulin antibody production; spleen cells exhibited slight activity, whereas thymus cells were incapable of inducing immune responses. Passively produced thyroiditis was characterized by mild inflammatory lesions. The incidence of delayed skin hypersensitivity in positive recipients was much higher than the occurrence of thyroiditis. Prolonged treatment of intact animals with immune or normal rat serum did not induce lesions typical of allergic thyroiditis. It was concluded that passive induction of experimental allergic thyroiditis can be accomplished in inbred Lewis rats by immunologically active lymphoid cells. The role of anti-thyroid antibodies in the pathogenesis of thyroiditis was discussed.