CD8 + T-cell responses in HIV controllers: potential implications for novel HIV remission strategies.

CD8 + T-cell responses in HIV controllers: potential implications for novel HIV remission strategies.
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DOI:
10.1097/coh.0000000000000748
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发表时间:
2022-09-01
影响因子:
4.1
通讯作者:
Trautmann, Lydie
Trautmann, Lydie
中科院分区:
医学3区
文献类型:
--
作者:
Rutishauser, Rachel L.;Trautmann, Lydie

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对自发性艾滋病毒和猴病毒控制者的免疫学研究发现,病毒特异性CD8+ T细胞是病毒控制的关键免疫机制。这篇综述的目的是考虑如何将与CD8+ T细胞控制自然感染的艾滋病毒/SIV相关的机制知识用于艾滋病毒缓解策略。我们讨论了CD8+ T细胞反应的特征,这些T细胞反应可能对抑制自发控制者中的艾滋病毒复制至关重要,包括艾滋病毒抗原识别(包括特定的人类白细胞抗原类型)、广泛交叉反应的T细胞受体和表位靶向、增强的扩张和抗病毒功能以及病毒特异性T细胞在宿主持久性部位附近的定位。我们还讨论了需要更好地了解在急性感染期间和治疗中断后与艾滋病毒/ 病毒控制相关的CD8+ T细胞反应的时间,以及HIV/SIV特异性CD8+CD8+T细胞与其他免疫反应协调以实现控制的机制。我们提出了关于如何将自然感染的这种知识应用于基于CD8+ T细胞的缓解策略的设计和评估的启示,并提出了需要考虑的问题,因为这些策略针对不同的CD8+ T细胞依赖的病毒控制机制。
Immunological studies of spontaneous HIV and simian virus (SIV) controllers have identified virus-specific CD8+ T cells as a key immune mechanism of viral control. The purpose of this review is to consider how knowledge about the mechanisms that are associated with CD8+ T cell control of HIV/SIV in natural infection can be harnessed in HIV remission strategies. We discuss characteristics of CD8+ T-cell responses that may be critical for suppressing HIV replication in spontaneous controllers comprising HIV antigen recognition including specific human leukocyte antigen types, broadly cross-reactive T cell receptors and epitope targeting, enhanced expansion and antiviral functions, and localization of virus-specific T cells near sites of reservoir persistence. We also discuss the need to better understand the timing of CD8+ T-cell responses associated with viral control of HIV/SIV during acute infection and after treatment interruption as well as the mechanisms by which HIV/SIV-specific CD8+ T cells coordinate with other immune responses to achieve control. We propose implications as to how this knowledge from natural infection can be applied in the design and evaluation of CD8+ T-cell-based remission strategies and offer questions to consider as these strategies target distinct CD8+ T-cell-dependent mechanisms of viral control.
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