CD4(+) T-cell depletion in HIV infection: mechanisms of immunological failure.
CD4(+) T-cell depletion in HIV infection: mechanisms of immunological failure.
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DOI：
10.1111/imr.12066
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发表时间：
2013-07
影响因子：
8.7
通讯作者：
Picker LJ
中科院分区：
文献类型：
--
作者：
Okoye AA;Picker LJ
获得性免疫缺陷综合征（AIDS）发病机制的标志是CD4+ T细胞群的进行性耗竭，其与细胞免疫的进行性损害和对机会性感染（OI）的易感性增加密切相关。未经治疗的人类免疫缺陷病毒（HIV）感染的疾病进展可能需要多年时间，最初假设是病毒介导的CD4+ T细胞缓慢破坏的结果。然而，现在已知大量的CD4+记忆T细胞破坏发生在感染的早期，几乎总是没有明显的免疫缺陷。在大多数个体中，这种最初的破坏被CD4+记忆T细胞再生所抵消，该再生将CD4+ T细胞的数量和功能保持在与明显免疫缺陷相关的阈值以上。然而，在慢性免疫激活和免疫失调的情况下发生的这种再生不会恢复所有功能重要的CD4+ T细胞群，并且长期不稳定。最终，CD4+记忆T细胞稳态失败，关键效应细胞群下降到预防OI所需的水平以下。因此，明显的免疫缺陷的发作似乎与CD4+记忆T细胞动力学密切相关，并反映了直接病毒致细胞病变性和持续免疫激活对CD4+记忆T细胞增殖、分化和存活的间接影响的复杂相互作用。
The hallmark of acquired immunodeficiency syndrome (AIDS) pathogenesis is a progressive depletion of CD4+ T-cell populations in close association with progressive impairment of cellular immunity and increasing susceptibility to opportunistic infections (OI). Disease progression in untreated human immunodeficiency virus (HIV) infection can take many years, and it was originally hypothesized to be a consequence of slow, viral-mediated CD4+ T-cell destruction. However, massive CD4+ memory T-cell destruction is now known to occur quite early in infection, almost always without overt immunodeficiency. In most individuals, this initial destruction is countered by CD4+ memory T-cell regeneration that preserves CD4+ T-cell numbers and functions above the threshold associated with overt immunodeficiency. This regeneration, which occurs in the setting of chronic immune activation and immune dysregulation does not, however, restore all functionally important CD4+ T-cell populations and is not stable over the long term. Ultimately, CD4+ memory T-cell homeostasis fails and critical effector populations decline below the level necessary to prevent OI. Thus, the onset of overt immune deficiency appears to be intimately linked with CD4+ memory T-cell dynamics and reflects the complex interplay of direct viral cytopathogenicity and the indirect effects of persistent immune activation on CD4+ memory T-cell proliferation, differentiation, and survival.
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