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Influence of Signal Transducer and Activator of Transcription-1 Signaling on Thyroid Morphology and Function

Department of Pathology (H.J.K., R.R., M.A.L.-S., C.Y.C., M.K., N.R.R., P.C.), The Johns Hopkins School of Medicine, and Feinstone Department of Molecular Microbiology and Immunology (N.R.R., P.C.), The Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland 21205; and Department of Bioregulation (K.S.), Leprosy Research Center, National Institute of Infectious Diseases, Tokyo 189-0002, Japan

Address all correspondence and requests for reprints to: Patrizio Caturegli, Johns Hopkins Medical Institutions, Department of Pathology, Ross Building, Room 632, 720 Rutland Avenue, Baltimore, Maryland 21205. E-mail: pcat{at}jhmi.edu.

Interferon (IFN)- has been involved in the pathogenesis of Hashimoto thyroiditis. It is a cytokine released by infiltrating mononuclear cells that mediates its actions mainly through signal transducer and activator of transcription-1 (STAT1) but also through other transcription factors. To dissect the effect of IFN on thyroid morphology and function, we crossed transgenic mice that express IFN specifically in the thyroid gland to mice deficient in STAT1. Lack of STAT1 ameliorated the abnormal thyroid morphology and the primary hypothyroidism typical of IFN transgenic mice but not the suppressed iodine accumulation. Interestingly, lack of STAT1 alone decreased iodine accumulation, seemingly through expression of TGFβ. These results indicate that STAT1 is required to mediate some but not all of the phenotypic changes induced by IFN and that it also regulates iodine accumulation via TGFβ signaling.