| First Author | Jin Z | Year | 2004 |
| Journal | Clin Immunol | Volume | 113 |
| Issue | 2 | Pages | 187-92 |
| PubMed ID | 15451476 | Mgi Jnum | J:93120 |
| Mgi Id | MGI:3055999 | Doi | 10.1016/j.clim.2004.06.008 |
| Citation | Jin Z, et al. (2004) Experimental autoimmune thyroiditis in nonobese diabetic mice lacking interferon regulatory factor-1. Clin Immunol 113(2):187-92 |
| abstractText | 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 Hashimoto's 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 IFNgamma production by splenocytes. Our results suggest that IRF-1 is not pivotal in EAT in NOD mice. |
