Induction of Bystander T Cell Proliferation by Viruses and Type I Interferon in Vivo

DOI Web Site 被引用文献19件
  • David F. Tough
    D. F. Tough and J. Sprent, Department of Immunology, IMM4, Scripps Research Institute, 10666 North Torrey Pines Road, La Jolla, California 92037, USA.
  • Persephone Borrow
    P. Borrow, Department of Neuropharmacology, IMM6, Scripps Research Institute, 10666 North Torrey Pines Road, La Jolla, California 92037, USA.
  • Jonathan Sprent
    D. F. Tough and J. Sprent, Department of Immunology, IMM4, Scripps Research Institute, 10666 North Torrey Pines Road, La Jolla, California 92037, USA.

抄録

<jats:p> T cell proliferation in vivo is presumed to reflect a T cell receptor (TCR)-mediated polyclonal response directed to various environmental antigens. However, the massive proliferation of T cells seen in viral infections is suggestive of a bystander reaction driven by cytokines instead of the TCR. In mice, T cell proliferation in viral infections preferentially affected the CD44 <jats:sup>hi</jats:sup> subset of CD8 <jats:sup>+</jats:sup> cells and was mimicked by injection of polyinosinic-polycytidylic acid [poly(I:C)], an inducer of type I interferon (IFN I), and also by purified IFN I; such proliferation was not associated with up-regulation of CD69 or CD25 expression, which implies that TCR signaling was not involved. IFN I [poly(I:C)]-stimulated CD8 <jats:sup>+</jats:sup> cells survived for prolonged periods in vivo and displayed the same phenotype as did long-lived antigen-specific CD8 <jats:sup>+</jats:sup> cells. IFN I also potentiated the clonal expansion and survival of CD8 <jats:sup>+</jats:sup> cells responding to specific antigen. Production of IFN I may thus play an important role in the generation and maintenance of specific memory. </jats:p>

収録刊行物

  • Science

    Science 272 (5270), 1947-1950, 1996-06-28

    American Association for the Advancement of Science (AAAS)

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