Abstract
We provide evidence that platelet factor 4 (PF4), but not the related chemokine neutrophil-activating polypeptide-2, induced highly purified human natural killer (NK) cells to produce interleukin (IL)-8 in a time- and dosage-dependent manner. This ability was retained even while PF4 was bound to heparin. PF4 increased the steady state level of IL-8 mRNA, likely implying a transcriptional effect of PF4. Stimulation of NK cells through the Fc receptor for immunoglobulin G-IIIA was found to synergistically increase the effect of PF4 on IL-8 production but did not affect IL-2-related activities such as cytotoxic activity and proliferation. Pertussis toxin did not block the PF4-derived IL-8 production in NK cells, but this response was sensitive to wortmannin, implicating a role of phosphatidylinositol 3-kinase in the intracellular signaling pathway triggered by PF4. Our results characterize a new capacity for PF4 and provide further evidence for the pivotal role of NK cells in the environment of inflammation.
Original language | English |
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Pages (from-to) | 590-597 |
Number of pages | 8 |
Journal | Journal of Leukocyte Biology |
Volume | 72 |
Issue number | 3 |
State | Published - Sep 1 2002 |
Keywords
- Chemokines
- FcγRIIIA
- Inflammation
ASJC Scopus subject areas
- Immunology and Allergy
- Immunology
- Cell Biology