Up-regulation of HIV coreceptors CXCR4 and CCR5 on CD4(+) T cells during human endotoxemia and after stimulation with (myco)bacterial antigens: the role of cytokines.
Up-regulation of HIV coreceptors CXCR4 and CCR5 on CD4(+) T cells during human endotoxemia and after stimulation with (myco)bacterial antigens: the role of cytokines.
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人类内毒素血症期间和用（分枝）细菌抗原刺激后CD4（+）T细胞上HIV辅助受体CXCR4和CCR5的上调：细胞因子的作用。
DOI：
10.1182/blood.v96.8.2649.h8002649_2649_2654
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发表时间：
2000
期刊：
影响因子：
20.3
通讯作者：
T. Poll
中科院分区：
文献类型：
--
作者：
N. Juffermans;W. Paxton;P. E. Dekkers;A. Verbon;E. Jonge;P. Speelman;S. Deventer;T. Poll
人类免疫缺陷病毒 (HIV) 感染患者的并发感染会刺激 HIV 复制。趋化因子受体 CXCR4 和 CCR5 可以充当 HIV 辅助受体。作者假设，并发感染通过 CXCR4 和 CCR5 的上调增加 HIV 载量。使用实验性内毒素血症作为感染模型，评估了 8 名注射脂多糖（LPS，4 ng/kg）的受试者的 HIV 辅助受体表达的变化。注射LPS后4至6小时，CD4(+) T细胞上CXCR4和CCR5的表达增加2至4倍。在体外全血中，LPS 诱导 CD4(+) T 细胞上 CXCR4 和 CCR5 表达呈时间和剂量依赖性增加。用结核分枝杆菌（脂阿拉伯糖甘露聚糖）或金黄色葡萄球菌（脂磷壁酸）或葡萄球菌肠毒素 B 的细胞壁成分刺激后，观察到类似的变化。LPS 增加了 T 向性 HIV 病毒株富含 CD4 的外周血单核细胞 (PBMC) 的病毒感染性。相比之下，M-tropic 病毒感染性降低，可能是因为 CCR5 配体细胞因子 RANTES 和 MIP-1beta 水平升高。体外 LPS 刺激的 CXCR4 和 CCR5 上调被抗 TNF 和抗 IFN γ 抑制。与重组 TNF 或 IFN γ 一起孵育模拟了 LPS 效应。抗白介素 10（抗 IL-10）可降低 CCR5 表达，但不影响 CXCR4。相应地，rIL-10 诱导 CCR5 上调，但不诱导 CXCR4 上调。 HIV感染期间的并发感染可能上调CD4(+) T细胞上的CXCR4和CCR5，至少部分是通过细胞因子的作用。这种感染可能有利于HIV对表达CXCR4的CD4(+)T细胞的选择性。 （血。2000；96：2649-2654）
Concurrent infections in patients with human immunodeficiency virus (HIV) infection stimulate HIV replication. Chemokine receptors CXCR4 and CCR5 can act as HIV coreceptors. The authors hypothesized that concurrent infection increases the HIV load through up-regulation of CXCR4 and CCR5. Using experimental endotoxemia as a model of infection, changes in HIV coreceptor expression were assessed in 8 subjects injected with lipopolysaccharide (LPS, 4 ng/kg). The expression of CXCR4 and CCR5 on CD4(+) T cells was increased 2- to 4-fold, 4 to 6 hours after LPS injection. In whole blood in vitro, LPS induced a time- and dose-dependent increase in the expression of CXCR4 and CCR5 on CD4(+) T cells. Similar changes were observed after stimulation with cell wall components of Mycobacterium tuberculosis (lipoarabinnomannan) or Staphylococcus aureus (lipoteichoic acid), or with staphylococcal enterotoxin B. LPS increased viral infectivity of CD4-enriched peripheral blood mononuclear cells (PBMCs) with a T-tropic HIV strain. In contrast, M-tropic virus infectivity was reduced, possibly because of elevated levels of the CCR5 ligand cytokines RANTES and MIP-1beta. LPS-stimulated up-regulation of CXCR4 and CCR5 in vitro was inhibited by anti-TNF and anti-IFN gamma. Incubation with recombinant TNF or IFN gamma mimicked the LPS effect. Anti-interleukin 10 (anti-IL-10) reduced CCR5 expression, without influencing CXCR4. In accordance, rIL-10 induced up-regulation of CCR5, but not of CXCR4. Intercurrent infections during HIV infection may up-regulate CXCR4 and CCR5 on CD4(+) T cells, at least in part via the action of cytokines. Such infections may favor selectivity of HIV for CD4(+) T cells expressing CXCR4. (Blood. 2000;96:2649-2654)
结核分枝杆菌对 HIV 复制的影响。
DOI：
--
发表时间：
1996
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Goletti,D;Weissman,D;Jackson,RW;Graham,NM;Vlahov,D;Klein,RS;Munsiff,SS;Ortona,L;Cauda,R;Fauci,AS
通讯作者：
Fauci,AS
DOI：
10.1093/infdis/175.1.118
发表时间：
1997
期刊：
The Journal of infectious diseases
影响因子：
--
作者：
T. V. D. Poll;R. D. W. Malefyt;S. Coyle;Stephen F. Lowry
通讯作者：
T. V. D. Poll;R. D. W. Malefyt;S. Coyle;Stephen F. Lowry