© The Rockefeller University Press, 0022-1007/1997/7/39/ $5.00
The Journal of Experimental Medicine, Volume 186, Number 1, July 7, 1997 39-45
Interleukin 12 (IL-12) Is Crucial to the Development of Protective Immunity in Mice Intravenously Infected with Mycobacterium tuberculosis
Andrea M. Cooper*,
Jeanne Magram
,
Jessica Ferrante
, and
Ian M. Orme*
From the * Department of Microbiology, Colorado State University, Fort Collins, Colorado 80523; and the
Department of Inflammation and Autoimmune Diseases, Hoffman-La Roche Incorporated, Nutley, New Jersey 07110
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-
(IFN-
), 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-
. 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-
and the activation of antigen-specific lymphocytes capable of creating a protective granuloma.
Address correspondence to Andrea M. Cooper, Department of Microbiology, Colorado State University, Fort Collins, Colorado 80524. Phone: 970-491-2833; FAX: 970-491-1815; E-mail: acooper{at}vines.colostate.edu
1Abbreviations used in this paper: DTH, delayed type hypersensitivity; ES, embryonic stem; HPRT, hypoxanthine phosphoribosyl transferase; PPD, purified protein derivative.

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Salkowski, C. A., Thomas, K. E., Cody, M. J., Vogel, S. N.
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Kawakami, K., Koguchi, Y., Qureshi, M. H., Miyazato, A., Yara, S., Kinjo, Y., Iwakura, Y., Takeda, K., Akira, S., Kurimoto, M., Saito, A.
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