Mice lacking bioactive IL-12 can generate protective, antigen-specific cellular responses to mycobacterial infection only if the IL-12 p40 subunit is present
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2002
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Recent evidence suggests that absence of the IL-12p40 subunit is more detrimental to the generation of protective responses than
is the absence of the p35 subunit. To determine whether this is the case in tuberculosis, both p35 and p40 knockout mice were
infected with Mycobacterium tuberculosis. Mice lacking the p40 subunit were highly susceptible to increased bacterial growth,
exhibited reduced production of IFN- , and had increased mortality. In contrast, mice lacking the p35 subunit exhibited a
moderate ability to control bacterial growth, were able to generate Ag-specific IFN- responses, and survived infection longer. The
superior Ag-specific responses of the p35 gene-disrupted mice, when compared with the p40 gene-disrupted mice, suggest that the p40
subunit may act other than as a component of IL-12. A candidate molecule capable of driving the protective responses in the p35
gene-disrupted mice is the novel cytokine IL-23. This cytokine is composed of the IL-12 p40 subunit and a p19 subunit. In support of
a role for this cytokine in protective responses to M. tuberculosis, we determined that the p19 subunit is induced in the lungs of infected
mice.
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COOPER, Andrea M. et al. Mice lacking bioactive IL-12 can generate protective, antigen-specific cellular responses to mycobacterial infection only if the IL-12 p40 subunit is present. The Journal of Immunology, Rockville, v. 168, p. 1322-1327, 2002.