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The 90K Protein Increases Major Histocompatibility Complex Class I Expression and Is Regulated by Hormones, -Interferon, and Double-Strand Polynucleotides

Cell Regulation Section (A.G., B.F., K.S., M.N., C.G., G.N., L.D.K.), Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892; Section of Medical Oncology (A.G., N.T., B.F., M.D.T., S.I.), Department of Oncology and Neurosciences and Section of Endocrinology (C.G., G.N.), Department of Medicine and Science of Aging, Università degli Studi G. D’Annunzio, Faculty of Medicine and Surgery, 66100 Chieti, Italy; Experimental Immunology Branch (D.S.S.), National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892; and Edison Biotechnology Institute (L.D.K.), Department of Biomedical Sciences, Ohio University College of Osteopathic Medicine, Athens, Ohio 45701

Address all correspondence and requests for reprints to: Stefano Iacobelli, M.D., Dipartimento di Oncologia e Neuroscienze, Sezione di Oncologia Medica, SEBI, via dei Vestini, 66100 Chieti, Italy. E-mail: iacobell{at}unich.it.

Here we report the cloning of the rat 90K, a homolog of the mouse cyclophilin C-associated protein/mouse adherent macrophage and human 90K. The protein is constitutively expressed by FRTL-5 thyrocytes, and its levels are modulated by TSH, insulin/IGF-I, and -interferon. Transfection of the cells with 90K cDNA or exposure to purified 90K resulted in a significant increase of the expression of major histocompatibility complex class I but not class II antigens. An increased expression of 90K was obtained after viral infection or introduction into the cells of fragments of viral, bacterial, or mammalian double-strand polynucleotides. The increase was sequence independent, not CpG mediated, and associated with the expression of molecules characterizing antigen-presenting-cell phenotype. The present data along with results from previous studies suggest that 90K plays an important role in the maintenance of an appropriate level of immune response.

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