Experimental autoimmune thyroiditis (EAT) is inducible in mice by immunization with thyroglobulin and adjuvant. Previous studies have shown that EAT is an autoimmune Th1-mediated disease but its characteristics differ with the adjuvant. Granulomatous lesions with marked follicular disruption develop following administration of thyroglobulin (Tg) and complete Freund's adjuvant (CFA) whereas when lipopolysaccharide (LPS) is used as the adjuvant only focal infiltrates of mononuclear cells are observed. The pro-inflammatory cytokine, TNF-alpha, is associated with Th1 autoimmune-mediated conditions. Cytokine antagonists have been used as potential therapeutic agents in several experimental autoimmune models. Soluble cytokine receptors belong to this category and may naturally be shed from cell membranes to inhibit cytokine activity. We show that the administration of the soluble TNF receptor type I (sTNFR I) in the induction of EAT has very different effects on the two models of induced autoimmune thyroiditis. sTNFR I treatment inhibits the induction of EAT only when mouse Tg is given with LPS not with CFA, suggesting an important difference in the pathogenic processes.
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