IL-4 and a glucocorticoid up-regulate CXCR4 expression on human CD4+ T lymphocytes and enhance HIV-1 replication

被引:82
作者
Wang, JB
Harada, A
Matsushita, S
Matsumi, S
Zhang, Y
Shioda, T
Nagai, Y
Matsushima, K
机构
[1] Univ Tokyo, Sch Med, Dept Mol Prevent Med, Bunkyo Ku, Tokyo 1130033, Japan
[2] Univ Tokyo, CREST, Tokyo 1130033, Japan
[3] Kanazawa Univ, Sch Med, Dept Hyg, Kanazawa, Ishikawa 920, Japan
[4] Kumamoto Univ, Sch Med, AIDS Res Ctr, Kumamoto 860, Japan
[5] Univ Tokyo, Inst Med Sci, Dept Virol, Tokyo, Japan
关键词
co-receptor; cytokine dexamethasone; immunosuppressive agents; AIDS;
D O I
10.1002/jlb.64.5.642
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
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 Tvas therefore studied. Th2 polarized cells expressed more CXCR4 than Th1 cells. Among a panel of cytokiues 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-1 alpha. 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.
引用
收藏
页码:642 / 649
页数:8
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