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Laboratory of Cancer Immunology, Department of Cryobiology and Cell Therapy, Cancer Research Institute, Barcelona, Spain
Correspondence: Fèlix Rueda, Laboratory of Cancer Immunology, Department of Cryobiology and Cell Therapy, Cancer Research Institute (IRO), Autovia de Castelldefels, Km 2.7, 08907 L’Hospitalet de Llobregat, Barcelona, Spain. E-mail: frueda{at}iro.es
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.
Key Words: inflammation • chemokines • Fc
RIIIA
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