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Cytokine‐mediated regulation of CXCR4 expression in human neutrophils
Author(s) -
Nagase Hiroyuki,
Miyamasu Misato,
Yamaguchi Masao,
Imanishi Masako,
Tsuno Nelson H.,
Matsushima Kouji,
Yamamoto Kazuhiko,
Morita Yutaka,
Hirai Koichi
Publication year - 2002
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.71.4.711
Subject(s) - cxc chemokine receptors , biology , cxcr4 , chemokine , stromal cell derived factor 1 , chemokine receptor , cytokine , stromal cell , microbiology and biotechnology , receptor , granulocyte , immunology , cxcl16 , inflammation , cancer research , biochemistry
Several lines of evidence have suggested that a CXC chemokine receptor 4 (CXCR4)/stromal cell‐derived factor‐1 [SDF‐1; CXC chemokine ligand 12 (CXCL12)] pair is involved in baseline trafficking of leukocytes into extravascular tissues and that modulation of surface CXCR4 expression may represent an alternative mechanism for control of cell‐specific biological responses to SDF‐1/CXCL12. We explored the regulation of CXCR4 expression by cytokines in polymorphonuclear neutrophils (PMNs). No significant surface expression of CXCR4 in freshly isolated PMNs was detected, but expression became apparent gradually during incubation. SDF‐1α/CXCL12 initiated Ca 2+ mobilization and migratory responses in 20 h cultured PMNs. The surface CXCR4 expression was suppressed most potently by interferon‐γ (IFN‐γ). IFN‐α, granulocyte‐macrophage colony‐stimulating factor (GM‐CSF), and G‐CSF also inhibited spontaneous CXCR4 expression. Real‐time, quantitative PCR experiments revealed that a spontaneous increase and an IFN‐γ‐mediated decrease in surface CXCR4 paralleled changes in the CXCR4 mRNA level. These results on PMNs support the argument that the SDF‐1 (CXCL12)/CXCR4 system is regulated by cell type‐specific mechanisms.