Premium
IL‐4 and a glucocorticoid up‐regulate CXCR4 expression on human CD4 + T lymphocytes and enhance HIV‐1 replication
Author(s) -
Wang Jianbin,
Harada Akihisa,
Matsushita Shuzo,
Matsumi Shintaro,
Zhang Yi,
Shioda Tatsuo,
Nagai Yoshiyuki,
Matsushima Kouji
Publication year - 1998
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 - 10.1002/jlb.64.5.642
Subject(s) - biology , glucocorticoid , cxcr4 , replication (statistics) , human immunodeficiency virus (hiv) , microbiology and biotechnology , viral replication , expression (computer science) , virology , immunology , immune system , chemokine , virus , computer science , programming language
CXCR4 is a key co‐receptor required for the infection of T‐tropic HIV‐1 strain of CD4 + T lymphocytes. The regulation of this chemokine receptor was therefore studied. Th2 polarized cells expressed more CXCR4 than Th1 cells. Among a panel of cytokines and stimulants, a Th2 type cytokine interleukin‐4 (IL‐4) selectively up‐regulated the mRNA level as well as surface protein expression of CXCR4 within 16 h. In addition, CXCR4 was also up‐regulated by a glucocorticoid, dexamethasone. These treated cells became more responsive in transendothelial migration assays to the specific CXCR4 ligand, SDF‐1α. Furthermore, up‐regulation of CXCR4 was also associated with the enhancement of HIV replication in human CD4 + T lymphocytes. This study indicates the enhanced T‐tropic HIV‐1 infection to CD4 + T lymphocytes through up‐regulation of CXCR4 by several immunomodulating agents, IL‐4, and a glucocorticoid. These findings may explain the shift to T‐tropic HIV‐1 dominance during AIDS progression when Th2 comes to predominate. J. Leukoc. Biol. 64: 642–649; 1998.