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Cutting Edge |
*
Department of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104;
Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892;
Medical Research Council Center for Immune Regulation, School of Medicine, University of Birmingham, Edgbaston, Birmingham, U.K.; and
Department of Medicine, Cornell–Division of Immunology, Cornell University Medical College, New York, NY 10021
The production of IL-12 is required for immunity to many
intracellular pathogens. Recent studies have shown that c-Rel, a member
of the NF-
B family of transcription factors, is essential for
LPS-induced IL-12p40 production by macrophages. In this study, we
demonstrate that c-Rel is also required for IL-12p40 production by
macrophages in response to Corynebacterium parvum, CpG
oligodeoxynucleotides, anti-CD40 and low molecular weight
hyaluronic acid. However, c-Rel-/- mice infected with
Toxoplasma gondii produce comparable amounts of IL-12p40
to infected wild-type mice and have an IL-12-dependent mechanism of
resistance to this infection. Furthermore, c-Rel was not required for
IL-12p40 production by macrophages or dendritic cells in response to
soluble Toxoplasma Ag, and neutrophils from
c-Rel-/- mice contain normal amounts of preformed
IL-12p40. Together these studies reveal the presence of c-Rel-dependent
pathways critical for IL-12p40 production in response to inflammatory
stimuli and demonstrate a novel c-Rel-independent pathway of IL-12p40
production during toxoplasmosis.
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