MRL-1pr/1pr mice are genetically predisposed to develop a systemic lup
us erythematosus-like syndrome that is clinically very similar to the
human disease. The results presented here demonstrate, for the first t
ime to our knowledge, that MRL-1pr/1pr mice also develop thyroiditis a
s part of their systemic autoimmune disorder. The thyroid gland was in
filtrated by immunocomponent cells with defined lymphoid follicular ce
nters and extensive interstitial lymphocytes dispersed throughout the
thyroid epithelium. All the diseased mice were hypothyroid with reduce
d, relative levels of thyroid hormone (free T-4) and elevated levels o
f thyroid-stimulating hormone (TSH). They also had high concentrations
of circulating IgG class autoantibodies directed against thyroglobuli
n, thyroperoxidase and double-stranded DNA. The MRL-+/+ age-matched al
lelic counterpart mice had relatively few lymphocytes in their thyroid
tissue, and normal levels of thyroxine and TSH. The nondiseased mice
also had undetectable levels of thyroid reactive autoantibodies tested
for by enzyme-linked immunosorbent assays. Collectively these finding
s document that the MRL-1pr/1pr mice spontaneously develop autoimmune
thyroiditis and can be used as a model for the study of thyroid-specif
ic autoimmunity.