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*
Medical Research Council Unit Immunology in Infectious Diseases, Department of Immunology, University of Cape Town, Cape Town, South Africa; and
Institute of Immunology, Faculty of Veterinary Medicine, University of Leipzig, Leipzig, Germany
IL-12p35-/-p40-/- mice are highly susceptible to Mycobacterium bovis bacillus Calmette-Guérin (BCG) or Mycobacterium tuberculosis infection. In this study IL-12p35-/- mice, which are able to produce endogenous IL-12p40, cleared M. bovis BCG and showed reduced susceptibility to pulmonary M. tuberculosis infection, which was in striking contrast to the outcome of mycobacterial infection in IL-12p35-/-p40-/- mice. Resistance in wild-type and IL-12p35-/- mice was accompanied by protective granuloma formation and Ag-specific delayed-type hypersensitivity responses, which were impaired in susceptible IL-12p35-/- p40-/- mice. Furthermore, IL-12p35-/- mice, but not IL-12p35-/-p40-/- mice, mounted Ag-specific Th1 and cytotoxic T cell responses. In vivo therapy with rIL-12p40 homodimer restored the impaired delayed-type hypersensitivity responses in M. bovis BCG-infected IL-12p35-/-p40-/- mice and reverted them to a more resistant phenotype. Together, these results show evidence for a protective and agonistic role of endogenous and exogenous IL-12p40 in mycobacterial infection, which is independent of IL-12p70.
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