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Lysophosphatidylcholine up‐regulates CXCR4 chemokine receptor expression in human CD4 T cells
Author(s) -
Han Ki Hoon,
Hong Kyung Hee,
Ko Jesang,
Rhee Kyong Suk,
Hong Myeong Ki,
Kim Jae Joong,
Kim You Ho,
Park Seung Jung
Publication year - 2004
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.1103563
Subject(s) - lysophosphatidylcholine , biology , chemokine , inflammation , cxcl2 , chemokine receptor , t cell , caffeic acid phenethyl ester , microbiology and biotechnology , stromal cell , cancer research , immunology , immune system , biochemistry , phospholipid , phosphatidylcholine , membrane , caffeic acid , antioxidant
Oxidized low‐density lipoprotein (OxLDL) is an inflammatory modulator in the atherosclerotic plaque. We examined the effect of lysophosphatidylcholine (lysoPC), a main phospholipid component of OxLDL, on inflammatory responses in human CD4 T cells. We found that lysoPC dose‐ and time‐dependently increased expression of CXCR4, the chemokine receptor on CD4 T cells. This increase was inhibited by caffeic acid phenethyl ester or SN50, nuclear factor‐κB inhibitors, and also by suppression of G2A expression, the specific receptor for lysoPC, using antisense oligonucleotide. lysoPC enhanced CD4 T cell chemotaxis in response to stromal cell‐derived factor‐1 (SDF‐1), the exclusive ligand for CXCR4. lysoPC also enhanced SDF‐1‐stimulated production of inflammatory cytokines interleukin‐2 and interferon‐γ by CD4 T cells activated by anti‐CD3 immunoglobulin G. In conclusion, this study demonstrates that lysoPC directly modulates inflammatory responses in human CD4 T cells. The data suggest that the presence of lysoPC and SDF‐1 in atherosclerotic lesions may trigger inflammatory responses mediated by CD4 T cells, which may play an important role in progression of atherosclerosis.