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From the Mucosal Immunity Section, Laboratory of Clinical Investigation, National Institutes of
Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892
Complement receptor type 3 (CR3, CD11b/CD18) serves as a receptor for a number of endogenous ligands and infectious organisms, and is involved in adhesion and host defense functions. Here, we report that signaling via CR3 plays an important role in regulating production
of interleukin-12 (IL-12), a key mediator of cell-mediated immunity (CMI). We demonstrate
with a variety of stimuli a dose-dependent, specific downregulation of IL-12 secretion by human monocytes in vitro after exposure to antibodies to CR3 (anti-CD11b and anti-CD18), as
well as to the natural CR3 ligands, iC3b, and Histoplasma capsulatum. CR3 antibodies also suppressed interferon-
(IFN-) production in cultures of human peripheral blood mononuclear
cells (PBMC). We determined that one mechanism by which CR3 antibodies may suppress IL-12 production is by the inhibition of IFN--induced tyrosine phosphorylation. Finally, in a
murine model of IL-12-dependent septic shock, we provide evidence that administration of
CR3 antibodies leads to suppression of IL-12 and IFN- in vivo. Our studies thus define a
novel role for CR3 in regulating CMI functions via IL-12.
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