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pubmed-article:9206995pubmed:abstractTextImmunity 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.lld:pubmed
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pubmed-article:9206995pubmed:articleTitleInterleukin 12 (IL-12) is crucial to the development of protective immunity in mice intravenously infected with mycobacterium tuberculosis.lld:pubmed
pubmed-article:9206995pubmed:affiliationDepartment of Microbiology, Colorado State University, Fort Collins, Colorado 80523, USA.lld:pubmed
pubmed-article:9206995pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:9206995pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
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