Experimental autoimmune thyroiditis in nonobese diabetic mice lacking interferon regulatory factor-1

Interferon regulatory factor-1 (IRF-1) is pivotal in the regulation of interferon (IFN)-mediated immune reactions, and studies suggest that IRF-1 is involved in the development of autoimmune diseases. IRF-1+/+, +/−, and −/− nonobese diabetic (NOD) mice were immunized with mouse thyroglobulin (mTg) to determine whether IRF-1 is required in experimental autoimmune thyroiditis (EAT), a murine model for Hashimotoʹs thyroiditis (HT). IRF-1-deficient mice developed EAT and anti-mTg antibodies comparable to IRF-1+/+ and +/− mice. Whereas both CD4+ and CD8+ T cells were found in thyroids of IRF-1+/+ mice, the latter was not in IRF-1−/− mice. Major histocompatibility complex class II antigen was comparably expressed in thyroids of IRF-1+/+ and −/− mice. Lack of IRF-1 resulted in decreased CD8+ T cell number in the spleen and reduced IFNγ production by splenocytes. Our results suggest that IRF-1 is not pivotal in EAT in NOD mice.