01874nas a2200361   4500000000100000008004100001260001300042653001200055653001500067653002400082653002100106653001100127653000900138653001900147653002100166653003100187653002400218653001800242653003600260100001300296700001300309700002100322700001300343700001200356700001300368700001200381700001600393245011400409300001200523490000800535520095500543022001401498       2009                            d  c2009 Jul10aAnimals10aChemokines10aGenes, MHC Class II10aInterferon-gamma10aIodine10aMice10aMice, Knockout10aMice, Transgenic10aSTAT1 Transcription Factor10aSignal Transduction10aThyroid Gland10aTransforming Growth Factor beta1 aKimura H1 aRocchi R1 aLandek-Salgado M1 aSuzuki K1 aChen CY1 aKimura M1 aRose NR1 aCaturegli P00aInfluence of signal transducer and activator of transcription-1 signaling on thyroid morphology and function.  a3409-160 v1503 a<p>Interferon (IFN)-gamma 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 gamma on thyroid morphology and function, we crossed transgenic mice that express IFN gamma 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 gamma transgenic mice but not the suppressed iodine accumulation. Interestingly, lack of STAT1 alone decreased iodine accumulation, seemingly through expression of TGFbeta. These results indicate that STAT1 is required to mediate some but not all of the phenotypic changes induced by IFN gamma and that it also regulates iodine accumulation via TGFbeta signaling.</p>  a1945-7170