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Disseminated tuberculosis in interferon gamma gene-disrupted mice.pdf (605.38 kB)

Disseminated tuberculosis in interferon gamma gene-disrupted mice.

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journal contribution
posted on 2018-06-05, 15:55 authored by Andrea M. Cooper, Dyana K. Dalton, Timothy A. Stewart, John P. Griffin, David G. Russell, Ian M. Orme
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.

Funding

This work was supported by National Institutes of Health grant AI-27288.

History

Citation

Journal of Experimental Medicine, 1993, 178 (6), pp. 2243-2247

Author affiliation

/Organisation/COLLEGE OF MEDICINE, BIOLOGICAL SCIENCES AND PSYCHOLOGY/School of Medicine/Department of Infection, Immunity and Inflammation

Version

  • VoR (Version of Record)

Published in

Journal of Experimental Medicine

Publisher

Rockefeller University Press

issn

0022-1007

eissn

1540-9538

Copyright date

1993

Available date

2018-06-05

Publisher version

http://jem.rupress.org/content/178/6/2243

Language

en

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