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* Laboratory of Endocrine Cell Biology, Department of Internal Medicine,
Department of Microbiology and Immunology, Chungnam National University School of Medicine, Daejon, Korea;
Department of Biology, Daejin University, Kyeonggido, Korea;
Korea Research Institute of Bioscience and Biotechnology, Taejon, Korea;
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Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea; and
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Department of Biomedical Sciences, Ohio University School of Osteopathic Medicine and Edison Biotechnology Institute, Athens, OH 45701
It has been suggested that class I and class II MHC are contributing factors for numerous diseases including autoimmune thyroid diseases, type 1 diabetes, rheumatoid arthritis, Alzheimer’s disease, and multiple sclerosis. The class II trans-activator (CIITA), which is a non-DNA-binding regulator of class II MHC transcription, regulates the constitutive and inducible expression of the class I and class II genes. FRTL-5 thyroid cells incubated in the presence of IFN-
have a significantly higher level of cell surface rat MHC class II RTI.B. However, the IFN--induced RT1.B expression was suppressed significantly in cells incubated in the presence of thyrotropin. Thyrotropin (TSH) represses IFN--induced CIITA expression by inhibiting type IV CIITA promoter activity through the suppression of STAT1 activation and IFN regulatory factor 1 induction. This study found that TSH induces transcriptional activation of the STAT3 gene through the phosphorylation of STAT3 and CREB activation. TSH induces SOCS-1 and SOCS-3, and TSH-mediated SOCS-3 induction was dependent on STAT3. The cell line stably expressing the wild-type STAT3 showed a higher CIITA induction in response to IFN- and also exhibited TSH repression of the IFN--mediated induction of CIITA. However, TSH repression of the IFN--induced CIITA expression was not observed in FRTL-5 thyroid cells, which stably expresses the dominant negative forms of STAT3, STAT3-Y705F, and STAT3-S727A. This report suggests that TSH is also engaged in immunomodulation through signal cross-talk with the cytokines in thyroid cells.
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