Murine B7-2, an alternative CTLA4 counter-receptor that costimulates T cell proliferation and interleukin 2 production.

DOI PDF 被引用文献20件
  • G J Freeman
    Dana-Farber Cancer Institute, Department of Medicine, Harvard Medical School, Boston, MA 02115.
  • F Borriello
    Dana-Farber Cancer Institute, Department of Medicine, Harvard Medical School, Boston, MA 02115.
  • R J Hodes
    Dana-Farber Cancer Institute, Department of Medicine, Harvard Medical School, Boston, MA 02115.
  • H Reiser
    Dana-Farber Cancer Institute, Department of Medicine, Harvard Medical School, Boston, MA 02115.
  • J G Gribben
    Dana-Farber Cancer Institute, Department of Medicine, Harvard Medical School, Boston, MA 02115.
  • J W Ng
    Dana-Farber Cancer Institute, Department of Medicine, Harvard Medical School, Boston, MA 02115.
  • J Kim
    Dana-Farber Cancer Institute, Department of Medicine, Harvard Medical School, Boston, MA 02115.
  • J M Goldberg
    Dana-Farber Cancer Institute, Department of Medicine, Harvard Medical School, Boston, MA 02115.
  • K Hathcock
    Dana-Farber Cancer Institute, Department of Medicine, Harvard Medical School, Boston, MA 02115.
  • G Laszlo
    Dana-Farber Cancer Institute, Department of Medicine, Harvard Medical School, Boston, MA 02115.

抄録

<jats:p>The B7-1 molecule, expressed on antigen presenting cells (APC), provides a crucial costimulatory signal for T cell activation. Recent studies demonstrate the existence of alternative, non-B7-1 CTLA4 counter-receptors in mice and humans. Here, we describe the molecular cloning and demonstrate costimulatory function of the murine B7-2 (mB7-2) gene. Murine B7-2 cDNA encodes a member of the Ig supergene family that binds CTLA4-Ig and stains with the GL1 but not anti-mB7-1 mAb. Murine B7-2 costimulates the proliferation and interleukin 2 production of CD4+ T cells and this costimulation can be inhibited by either CTLA4-Ig or GL1 mAb. Identification of the B7-2 molecule will permit further manipulation of the B7:CD28/CTLA4 costimulatory pathway which has been shown to be involved in the prevention of tolerance, induction of tumor immunity, and most recently, in the pathogenesis of autoimmunity.</jats:p>

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