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Department of Immunology, Schering-Plough Research Institute, Kenilworth, NJ 07033
We report that the addition of human macrophage inflammatory
protein-3ß (MIP-3ß) to cultures of human PBMCs that have been
activated with LPS or PHA results in a significant enhancement of IL-10
production. This effect was concentration-dependent, with optimal
MIP-3ß concentrations inducing more than a 5-fold induction of IL-10
from LPS-stimulated PBMCs and a 2- to 3-fold induction of IL-10 from
PHA-stimulated PBMCs. In contrast, no significant effect on IL-10
production was observed when 6Ckine, the other reported ligand for
human CCR7, or other CC chemokines such as monocyte chemoattractant
protein-1, RANTES, MIP-1
, and MIP-1ß were added to LPS- or
PHA-stimulated PBMCs. Similar results were observed using activated
purified human peripheral blood monocytes or T cells. Addition of
MIP-3ß to nonactivated PBMCs had no effect on cytokine production.
Enhancement of IL-10 production by MIP-3ß correlated with the
inhibition of IL-12 p40 and TNF- production by monocytes and with
the impairment of IFN-
production by T cells, which was reversed by
addition of anti-IL-10 Abs to the cultures. The ability of MIP-3ß
to augment IL-10 production correlated with CCR7 mRNA expression and
stimulation of intracellular calcium mobilization in both monocytes and
T cells. These data indicate that MIP-3ß acts directly on human
monocytes and T cells and suggest that this chemokine is unique among
ligands binding to CC receptors due to its ability to modulate
inflammatory activity via the enhanced production of the
anti-inflammatory cytokine IL-10.
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