Triple bypass: complicated paths to HIV escape.

Triple bypass: complicated paths to HIV escape.
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DOI:
10.1084/jem.20072371
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发表时间:
2007-11-26
期刊:
The Journal of experimental medicine
影响因子:
--
通讯作者:
McMichael AJ
McMichael AJ
中科院分区:
其他
文献类型:
--
作者:
McMichael AJ

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人类免疫缺陷病毒(HIV)1型在逃避免疫反应和持续存在方面非常有效,最终在一些患者中导致致命的免疫缺陷。细胞溶解CD8+T细胞(CTL)识别的表位突变就是这样一种逃逸过程。一项新的研究表明,HIV-1的一个逃逸突变也可能导致树突状细胞(DC)活性受损,可能会削弱后来的T细胞对相同和其他表位的反应。这些新的数据完善了我们对人类组织相容白细胞抗原(HLA)-B27呈递的免疫优势GAG表位逃避CTL反应的机制的理解。完全逃脱的复杂性有助于解释为什么这种HLA型患者进展到艾滋病的速度比平均速度慢。
Human immunodeficiency virus (HIV) type 1 is highly efficient at evading immune responses and persisting, ultimately causing fatal immunodeficiency in some patients. Mutation in the epitopes recognized by cytolytic CD8+ T cells (CTLs) is one such escape process. A new study now shows that one HIV-1 escape mutation may also result in impaired dendritic cell (DC) activity, possibly impairing later T cell responses to the same and other epitopes. The new data complete our understanding of the mechanisms by which the CTL response to an immunodominant gag epitope presented by human histocompatibility leukocyte antigen (HLA)-B27 is evaded. The complexity of the full escape helps to explain why patients with this HLA type progress to AIDS more slowly than average.
HIV-1 GAG中的簇突变是逃避HLA-B27限制的细胞毒性T淋巴细胞反应所必需的。
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