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From the * Department of Microbiology, Colorado State University, Fort Collins, Colorado 80523;
and the 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- Department of Inflammation and Autoimmune Diseases, Hoffman-La Roche Incorporated,
Nutley, New Jersey 07110
(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.
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