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Loss of CD127 expression links immune activation and CD4(+) T cell loss in HIV infection

机译:CD127表达的损失与艾滋病毒感染中的免疫激活和CD4(+)T细胞损失有关

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摘要

Although chronic immune activation correlates with CD4(+) T cell loss in HIV infection, an understanding of the factors mediating T cell depletion remains incomplete. We propose that reduced expression of CD127 (IL-7 receptor alpha chain, IL-7Ralpha), induced by immune activation, contributes to CD4(+) T cell loss in HIV infection. In particular, loss of CD127 on central memory CD4(+) T cells (T(CM)) severely restrains the regenerative capacity of the memory component of the immune system, resulting in a limited ability to control T cell homeostasis. Studies from both pathogenic and controlled HIV infection indicate that the containment of immune activation and preservation of CD127 expression are critical to the stability of CD4(+) T cells in infection. A better understanding of the factors regulating CD127 expression in HIV disease, particularly on T(CM) cells, might unveil new approaches exploiting the IL-7/IL-7R receptor pathway to restore T cell homeostasis and promote immune reconstitution in HIV infection.
机译:尽管慢性免疫激活与HIV感染中CD4(+)T细胞的丢失相关,但对介导T细胞耗竭因素的理解仍然不完全。我们建议减少表达的CD127(IL-7受体alpha链,IL-7Ralpha),由免疫激活引起,有助于在HIV感染中CD4(+)T细胞的丢失。特别是,中央记忆CD4(+)T细胞(T(CM))上CD127的丢失严重限制了免疫系统记忆成分的再生能力,从而导致控制T细胞稳态的能力受到限制。来自病原性和受控HIV感染的研究表明,免疫激活的抑制和CD127表达的保存对于CD4(+)T细胞在感染中的稳定性至关重要。更好地理解调节HIV疾病中CD127表达的因素,尤其是T(CM)细胞上的CD127的表达,可能会揭示利用IL-7 / IL-7R受体途径恢复T细胞稳态并促进HIV感染中免疫重建的新方法。

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