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-Primed and Lipopolysaccharide-Challenged Human Monocytes1
*
Department of Dermatology and Allergology, Hannover Medical University, Hannover, Germany; and
Department of Immunology, University of Göttingen, Göttingen, Germany
IL-12 is a key mediator of the immune response, skewing T
lymphocytes toward a type 1 cytokine pattern. Priming with IFN-
or
GM-CSF is required for expression of IL-12p70 by cells in which IL-12
is inducible by bacterial products such as LPS. We here show for the
first time that the production of bioactive IL-12 by human monocytes
can be significantly suppressed by C5a if applied to IFN--primed
monocytes before LPS stimulation. There was a dose-dependent
suppression by IL-12 (p70) on the levels of intracellular cytokine
production and cytokine secretion. mRNA studies consistently showed a
reduction of IL-12p40 and IL-12p35 expression by stimulation in the
presence of C5a. The results of several different experimental
approaches suggest that IL-12 down-regulation was not due to endogenous
IL-10, IL-4, or PGE2 production induced by C5a. Moreover,
stimulation of IFN--primed monocytes with C5a did not lead to a
down-regulation of the CD14 Ag, which is an LPS receptor. These
findings show that the anaphylatoxin C5a has the capacity to directly
interact with the complex regulation of IL-12.
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