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      Disseminated tuberculosis in interferon gamma gene-disrupted mice

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      The Journal of Experimental Medicine
      The Rockefeller University Press

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          Abstract

          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.

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          Author and article information

          Journal
          J Exp Med
          The Journal of Experimental Medicine
          The Rockefeller University Press
          0022-1007
          1540-9538
          1 December 1993
          : 178
          : 6
          : 2243-2247
          Article
          94065594
          10.1084/jem.178.6.2243
          2191280
          8245795
          109d97f0-08c4-4076-9f08-5749d6ade745
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          Medicine
          Medicine

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