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Submitted on March 9, 2005
Accepted on April 18, 2005
)
Department of Pathology, The Johns Hopkins School of Medicine, Baltimore, MD; Department of Microbiology, Leprosy Research Center, National Institute of Infectious Diseases, Tokyo, 189-0002 Japan; National Hormone and Peptide Program, Harbor-UCLA Medical Center, Torrance, CA; Feinstone Department of Molecular Microbiology and Immunology, The Johns Hopkins Bloomberg School of Public Health, Baltimore, MD
* To whom correspondence should be addressed. E-mail: pcat{at}jhmi.edu.
Interleukin-12 (IL-12), a prototypic T helper 1 cytokine, has been implicated in the pathogenesis of organ-specific autoimmune diseases such as Hashimoto's thyroiditis, but reported to give conflicting results in murine models of lymphocytic thyroiditis. To determine the effects of chronic, local production of IL-12 within the thyroid gland, we created transgenic mice that express IL-12 p70 under the transcriptional control of the thyroglobulin promoter. Transgenics developed growth retardation, moderate primary hypothyroidism, and mild lymphocytic infiltration of the thyroid gland. The hypothyroidism was associated with increased mRNA levels of the sodium-iodide symporter, an increase partly due to a direct effect of IL-12 on the thyrocyte. Upon immunization with a suboptimal doses of mouse thyroglobulin, IL-12 transgenic mice developed a lymphocytic thyroiditis that was more frequent and severe than that observed in wild-type littermates. The disease-promoting effect of IL-12 was independent of IFN
, as shown by the similar IFN levels in transgenics and controls. These findings highlight the contrasting roles of two T helper 1 cytokines, and report a novel role of IL-12 on thyroid hormonogenesis.
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