Cooper AM, Magram J, Ferrante J, and Orme IM. Interleukin 12 (IL-12) is crucial to the development of protective immunity in mice intravenously infected with Mycobacterium tuberculosis. J Exp Med 186:39-45

Department of Microbiology, Colorado State University, Fort Collins, Colorado 80523, USA.
Journal of Experimental Medicine (Impact Factor: 13.91). 08/1997; 186(1):39-45. DOI: 10.1084/jem.186.1.39
Source: PubMed

ABSTRACT Immunity to Mycobacterium tuberculosis infection is associated with the emergence of protective CD4 T cells that secrete cytokines, resulting in activation of macrophages and the recruitment of monocytes to initiate granuloma formation. The cytokine-mediating macrophage activation is interferon-gamma (IFN-gamma), which is largely dependent on interleukin-12 (IL-12) for its induction. To address the role of IL-12 in immunity to tuberculosis, IL-12 p40(-/-) mice were infected with M. tuberculosis and their capacity to control bacterial growth and other characteristics of their immune response were determined. The IL-12 p40(-/-) mice were unable to control bacterial growth and this appeared to be linked to the absence of both innate and acquired sources of IFN-gamma. T cell activation as measured by delayed type hypersensitivity and lymphocyte accumulation at the site of infection were both markedly reduced in the IL-12 p40(-/-) mice. Therefore, IL-12 is essential to the generation of a protective immune response to M. tuberculosis, with its main functions being the induction of the expression of IFN-gamma and the activation of antigen-specific lymphocytes capable of creating a protective granuloma.

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Available from: Andrea M Cooper, Aug 26, 2015
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    • "IL-12 is induced in macrophages and DCs after activation by microbial TLR ligands and other cytokines. Experiments using IL-12 deficient mice show an increase in bacterial burden and a drastic reduction in host survival (Flynn et al., 1995b; Cooper et al., 1997). These studies established IL-12 as a crucial cytokine in the development and maintenance of the type-1 cellular response to M.tb infection . "
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