CD4+ T cell depletion in human immunodeficiency virus (HIV) infection: role of apoptosis.

CD4+ T cell depletion in human immunodeficiency virus (HIV) infection: role of apoptosis.
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DOI:
10.3390/v3050586
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发表时间:
2011-05
期刊:
Viruses
影响因子:
--
通讯作者:
Rebollo A
Rebollo A
中科院分区:
其他
文献类型:
--
作者:
Février M;Dorgham K;Rebollo A

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人类免疫缺陷病毒(HIV)感染主要是一种粘膜疾病,胃肠道(GI)是HIV复制的主要部位。CD4+ T细胞的丢失和系统性免疫超活化是HIV感染的标志。急性感染的结束与特异性CD4+和CD8+ T细胞应答的出现以及感染慢性期的建立相关。尽管病毒血症的稳态水平较低,但免疫激活和炎症的异常水平仍然存在。虽然持续性免疫超活化的原因仍然不完全的特点,胃肠道的生理变化可能发挥了重要作用。肠道相关淋巴组织(GALT)中Th17细胞的恢复失败可能会损害肠道粘膜屏障的恢复。本文就CD4+ T细胞耗竭对HIV发病机制的影响作一综述。
Human immunodeficiency virus (HIV) infection is principally a mucosal disease and the gastrointestinal (GI) tract is the major site of HIV replication. Loss of CD4+ T cells and systemic immune hyperactivation are the hallmarks of HIV infection. The end of acute infection is associated with the emergence of specific CD4+ and CD8+ T cell responses and the establishment of a chronic phase of infection. Abnormal levels of immune activation and inflammation persist despite a low steady state level of viremia. Although the causes of persistent immune hyperactivation remain incompletely characterized, physiological alterations of gastrointestinal tract probably play a major role. Failure to restore Th17 cells in gut-associated lymphoid tissues (GALT) might impair the recovery of the gut mucosal barrier. This review discusses recent advances on understanding the contribution of CD4+ T cell depletion to HIV pathogenesis.
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