Disseminated tuberculosis in interferon gamma gene-disrupted mice.

DOI PDF 被引用文献33件
  • A M Cooper
    Department of Microbiology, Colorado State University, Fort Collins 80523.
  • D K Dalton
    Department of Microbiology, Colorado State University, Fort Collins 80523.
  • T A Stewart
    Department of Microbiology, Colorado State University, Fort Collins 80523.
  • J P Griffin
    Department of Microbiology, Colorado State University, Fort Collins 80523.
  • D G Russell
    Department of Microbiology, Colorado State University, Fort Collins 80523.
  • I M Orme
    Department of Microbiology, Colorado State University, Fort Collins 80523.

抄録

<jats:p>The expression of protective immunity to Mycobacterium tuberculosis in mice is mediated by T lymphocytes that secrete cytokines. These molecules then mediate a variety of roles, including the activation of parasitized host macrophages, and the recruitment of other mononuclear phagocytes to the site of the infection in order to initiate granuloma formation. Among these cytokines, interferon gamma (IFN-gamma) is believed to play a key role is these events. In confirmation of this hypothesis, we show in this study that mice in which the IFN-gamma gene has been disrupted were unable to contain or control a normally sublethal dose of M. tuberculosis, delivered either intravenously or aerogenically. In such mice, a progressive and widespread tissue destruction and necrosis, associated with very high numbers of acid-fast bacilli, was observed. In contrast, despite the lack of protective immunity, some DTH-like reactivity could still be elicited. These data, therefore, indicate that although IFN-gamma may not be needed for DTH expression, it plays a pivotal and essential role in protective cellular immunity to tuberculosis infection.</jats:p>

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