TY - JOUR
T1 - Platelet factor 4 induces human natural killer cells to synthesize and release interleukin-8
AU - Martí, Francesc
AU - Bertran, Esther
AU - Llucià, Montserrat
AU - Villén, Esther
AU - Peiró, Matilde
AU - Garcia, Joan
AU - Rueda, Fèlix
PY - 2002/9/1
Y1 - 2002/9/1
N2 - 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.
AB - 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.
KW - Chemokines
KW - FcγRIIIA
KW - Inflammation
UR - http://www.scopus.com/inward/record.url?scp=0036745072&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0036745072&partnerID=8YFLogxK
U2 - 10.1189/jlb.72.3.590
DO - 10.1189/jlb.72.3.590
M3 - Article
C2 - 12223528
AN - SCOPUS:0036745072
SN - 0741-5400
VL - 72
SP - 590
EP - 597
JO - Journal of Leukocyte Biology
JF - Journal of Leukocyte Biology
IS - 3
ER -