Abnormalities in the SJL mouse provide evidence for different mechanisms for the induction and transfer of tolerance to mouse thyroglobulin.

Experimental autoimmune thyroiditis (EAT) induced by immunization of susceptible (H-2k) mice can be significantly suppressed by pretreatment with soluble mouse thyroglobulin administered intravenously. Lightly irradiated recipients of spleen cells from donors pretreated in this way show a reduced response when subsequently challenged with mouse thyroglobulin and adjuvant (Kong et al., 1982; Parish et al., 1988). Previous studies on the SJL mouse revealed, among other abnormalities, a lack of suppressor cells (Cooke & Hutchings, 1984; Hutchings, Varey & Cooke, 1986; Amagai & Cinader, 1981) and therefore tolerance induction to mouse thyroglobulin and subsequent transfer was examined in these animals. The SJL mouse could be tolerized by i.v. administration of mouse thyroglobulin, but transfer of spleen cells from these animals failed to mediate suppression in syngeneic recipients. Several congenic strains of B10 mice showed similar 'in situ' tolerance without subsequent successful transfer and we conclude that the tolerance system described may be mediated by two distinct pathways and that the SJL appears to be defective only in the second pathway. Studies on other mouse strains suggest that the ability to be tolerized or to transfer tolerance is not dependent on a particular H-2 or I-E.