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beta(2)-microglobulin-deficient background ameliorates lethal phenotype of the TGF-beta 1 null mouse

  1. Author:
    Kobayashi, S.
    Yoshida, K.
    Ward, J. M.
    Letterio, J. J.
    Longenecker, G.
    Yaswen, L.
    Mittleman, B.
    Mozes, E.
    Roberts, A. B.
    Karlsson, S.
    Kulkarni, A. B.

  2. Author Address

    Kulkarni AB Natl Inst Dent & Craniofacial Res, Funct Genom Unit, NIH Gene Targeting Facil,Bldg 30,Room 529,30 Convent Bethesda, MD 20892 USA Natl Inst Dent & Craniofacial Res, Funct Genom Unit, NIH Bethesda, MD 20892 USA NINDS, Dev & Metab Neurol Branch, NIH Bethesda, MD 20892 USA NCI, Vet & Tumor Pathol Sect, Off Lab Anim Sci, NIH Frederick, MD 21702 USA NCI, Lab Cell Regulat & Carcinogenesis, NIH Bethesda, MD 20892 USA NCI, Expt Immunol Branch, NIH Bethesda, MD 20892 USA Weizmann Inst Sci, Dept Immunol IL-76100 Rehovot Israel
    1. Year: 1999
  2. Journal: Journal of Immunology
    1. 163
    2. 7
    3. Pages: 4013-4019
  4. Type of Article: Article
  1. Abstract:

    TGF-beta 1 null (TGF-beta 1(-/-)) mice die at 3-4 wk of age and show an autoimmune inflammatory phenotype associated with enhanced expression of both class I and II MHC molecules, To determine the role of MHC class I Ags in the autoimmune manifestations and the inflammation observed in TGF-beta 1(-/-) mice, we generated TGF-beta 1(-/-) mice in the genetic background of beta(2)-microglobulin deficiency (beta(2)M(-/-)). TGF-beta 1(-/-);beta(2)M(-/-) mice had improved survival compared with TGF-beta 1(-/-) mice. Histopathological examination showed less severe inflammation, especially in the heart, where Mac-2 reactive macrophages were significantly decreased as compared with TGF-beta 1(-/-) mice. In vivo depletion of CD8(+) T cells in TGF-beta 1(-/-) mice confirmed suppression of inflammation and reduction in the severity of the wasting syndrome. MHC class IT mRNA expression in TGF-beta 1(-/-);beta(2)M(-/-) mice was also lower than that in TGF-beta 1(-/-) mice, suggesting reduced systemic inflammation. Autoimmune response as judged by serum Ab titers to ssDNA and 16/6 Id and by immune complex deposits in kidney was reduced in TGF-beta 1(-/-);beta(2)M(-/-) mice, when compared with that in TGF-beta 1(-/-) mice. Our data thus indicate that MHC class I molecules influence the development of the autoimmunity and the inflammation seen in TGF-beta 1(-/-) mice and CD8(+) T cells may have a contribution to the inflammation in TGF-beta 1(-/-) mice. [References: 57]

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