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Lupus
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Characterization of autoimmune thyroiditis in MRL-lpr/lpr mice

L.M. Green

JL Pettis Veterans Medical Center, Department of Research-151, 11201 Benton Street, Loma Linda, CA 92357, Department of Microbiology/Physiology, Loma Linda University Medical School

M. LaBue

Department of Microbiology, Loma Linda University Medical School

J.P. Lazarus

Department of Physiology, Loma Linda University Medical School

K.K. Colburn

Department of Medicine, JL Pettis Vetarans Medical Center and Loma Linda University Medical School. Loma Linda, CA 92350. USA

MRL-lpr/lpr mice are genetically predisposed to develop a systemic lupus erythematosus-like syndrome that is clinically very similar to the human disease. The results presented here demonstrate, for the first time to our knowledge, that MRL-lpr/lpr mice also develop thyroiditis as part of their systemic autoimmune disorder. The thyroid gland was infiltrated by immunocomponent cells with defined lymphoid follicular centers and extensive interstitial lymphocytes dispersed throughout the thyroid epithelium. All the diseased mice were hypothyroid with reduced, relative levels of thyroid hormone (free T4) and elevated levels of thyroid-stimulating hormone (TSH). They also had high concentrations of circulating IgG class autoantibodies directed against thyroglobulin, thyroperoxidase and double-stranded DNA. The MRL-+/+ age-matched allelic counterpart mice had relatively few lymphocytes in their thyroid tissue, and normal levels of thyroxine and TSH. The non-diseased mice also had undetectable levels of thyroid reactive autoantibodies tested for by enzyme-linked immunosorbent assays. Collectively these findings document that the MRL-lpr/lpr mice spontaneously develop autoimmune thyroiditis and can be used as a model for the study of thyroid-specific autoimmunity.

Key Words: MRL-lpr/lpr mice • autoimmune thyroiditis • thyroperoxidase

Lupus, Vol. 4, No. 3, 187-196 (1995)
DOI: 10.1177/096120339500400305
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This article has been cited by other articles:


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Ann Rheum Dis, March 1, 2000; 59(3): 230 - 232.
[Abstract] [Full Text]


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