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* Department of Immunology and Cell Biology, Research Center Borstel, Borstel, Germany; and
Department of Experimental Pneumology, University Hospital Bergmannsheil, Bochum, Germany
Platelet factor 4 (PF-4), a platelet-derived CXC chemokine, has
been shown to induce the differentiation of monocytes into a subset of
macrophages that lack the expression of HLA-DR Ag. This suggests a
potential role for PF-4 in the modulation of monocyte-dependent T cell
activation. Using an Ag-specific stimulation model in which T cells
were cocultured with monocytes in the presence of recall Ags, we could
show that under these conditions PF-4-treatment caused a strong
decrease of T cell proliferation as well as of IFN-
release.
However, inhibition of T cell functions such as proliferation, IL-2
release, and IL-2 mRNA production did also occur when isolated T cells
were activated in the absence of monocytes with immobilized Abs
directed against CD3 in combination with cross-linked anti-CD28
Abs. The effect could be reversed when low concentrations of exogenous
IL-2 instead of anti-CD28 were used as a costimulus in combination
with anti-CD3 Abs. Further evidence for direct modulation of T cell
function by PF-4 was obtained by the detection of specific binding
sites for the chemokine on the surface of these cells. Taken together,
our results show that specific binding of PF-4, resulting in the
down-regulation of the IL-2-release correlates with the inhibition of
functions in activated T cells.
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