Interleukin-2 up-regulates expression of the human immunodeficiency virus fusion coreceptor CCR5 by CD4+ lymphocytes in vivo

被引:42
|
作者
Weissman, D
Dybul, M
Daucher, MB
Davey, RT
Walker, RE
Kovacs, JA
机构
[1] Univ Penn, Div Infect Dis, Philadelphia, PA 19104 USA
[2] NIAID, Immunoregulat Lab, Bethesda, MD 20892 USA
[3] Natl Inst Hlth, Ctr Clin, Dept Crit Care Med, Bethesda, MD USA
来源
JOURNAL OF INFECTIOUS DISEASES | 2000年 / 181卷 / 03期
关键词
D O I
10.1086/315303
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Intermittent interleukin-2 (IL-2) therapy can substantially increase CD4(+) T cell counts of human immunodeficiency virus (HIV)-infected subjects. Administration of IL-2 led to transient up-regulation of CCR5 on CD4(+) T cells; up to 87% of CD4(+) cells expressed CCR5 after a 5-day cycle, with return to baseline levels within 2 weeks. Unlike in vitro studies, CCR5 was coexpressed with CD45RA and CXCR4 on CD4(+) T cells after IL-2 therapy. The observed increase in coreceptor expression was nor associated with detectable increases in viral replication. IL-2 therapy induced CCR5 expression in >90% of circulating memory CD4(+) T cells, determined to be a long-term reservoir of HIV, suggesting significant activation of these cells. These studies demonstrate that levels of expression of HIV coreceptors alone do not always correlate with HIV replication in vivo and that IL-2 therapy activates a majority of memory T cells in the circulation and likely throughout the immune system.
引用
收藏
页码:933 / 938
页数:6
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