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,
Departments of
*
Microbiology and Immunology and
Physiology, Faculty of Medicine and Dentistry, University of Western Ontario, London, Ontario, Canada; and
Laboratory of Molecular Immunology and Inflammation and
§
The John P. Robarts Research Institute, London, Ontario, Canada
Staphylococcal superantigens (SAgs) are very potent T cell
mitogens, but they can also activate monocytes by binding directly to
MHC class II molecules in a manner independent of TCR coengagement.
Induction of proinflammatory cytokines and chemokine expression in
monocytes by superantigens has recently been reported. Here we report
that superantigen stimulation of human peripheral blood monocytes
results in a rapid, dose-dependent, and specific down-regulation of
chemokine (macrophage inflammatory protein-1
(MIP-1), monocyte
chemotactic protein-1 and MIP-1ß) binding sites (e.g., CCR1, CCR2,
and CCR5), which correlates with a concomitant hyporesponsiveness of
human monocytes to these CC chemokine ligands. This down-regulation
occurs 15–30 min following superantigen stimulation and is specific to
chemokine receptors, in that binding and responsiveness of monocytes to
the chemoattractant formyl-tripeptide FMLP are not affected. We further
demonstrate that SAg-induced down-modulation of chemokine binding and
monocyte hyporesponsiveness to the chemokines MIP-1, monocyte
chemotactic protein-1, and MIP-1ß is mediated through cellular
protein tyrosine kinases, and the down-modulation can be mimicked by an
MHC class II-specific mAb. Additionally, our observations indicate that
SAg-induced loss of chemokine binding and monocyte responsiveness is
probably mediated by secreted serine proteinases. Bacterial SAg-induced
down-modulation of chemokine responsiveness represents a previously
unrecognized strategy by some bacteria to subvert immune responses by
affecting the intricate balance between chemokine and chemokine
receptor expression and function.
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