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树突状细胞中 HIV-1 感染的先天信号传导。

Innate signaling in HIV-1 infection of dendritic cells.

机构信息

Center for Experimental and Molecular Medicine and Center for Infection and Immunity Amsterdam, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.

出版信息

Curr Opin HIV AIDS. 2011 Sep;6(5):348-52. doi: 10.1097/COH.0b013e328349a2d1.

Abstract

PURPOSE OF REVIEW

This review summarizes the current knowledge of innate signaling events that are involved in HIV-1 infection. We here focus on dendritic cells, which are among the first cells that encounter HIV-1 after exposure.

RECENT FINDINGS

HIV-1 triggers multiple pattern recognition receptors on dendritic cells that facilitate infection and transmission to T cells. Triggering of the C-type lectin DC-SIGN induces signals that promote HIV-1 replication in dendritic cells and transmission to T cells. Similarly, dendritic cell immunoreceptor has been shown to bind HIV-1 and facilitate transmission to T cells. The cytosolic sensors TRIM5 and cyclophilin A recognize capsid proteins and activate antiviral responses to prevent HIV-1 infection. Moreover, activation of mammalian target of rapamycin (mTOR) by HIV downregulates autophagy preventing adaptive immune responses.

SUMMARY

Dendritic cells express an array of pattern recognition receptors that are involved in HIV-1 infection. However, HIV-1 dampens signaling by these receptors leading to suppressed responses or takes advantage of their signaling for its own benefit.

摘要

目的综述

本文总结了固有信号事件在 HIV-1 感染中的作用。我们主要关注树突状细胞,它们是接触 HIV-1 的首批细胞之一。

最近的发现

HIV-1 可触发树突状细胞上的多种模式识别受体,促进感染和向 T 细胞的传播。C 型凝集素 DC-SIGN 的激活可诱导信号,促进树突状细胞中的 HIV-1 复制和向 T 细胞的传播。同样,已证实树突状细胞免疫受体可结合 HIV-1 并促进向 T 细胞的传播。胞质传感器 TRIM5 和亲环素 A 识别衣壳蛋白并激活抗病毒反应,以防止 HIV-1 感染。此外,HIV 激活雷帕霉素的哺乳动物靶标(mTOR)会下调自噬,从而阻止适应性免疫反应。

总结

树突状细胞表达一系列参与 HIV-1 感染的模式识别受体。然而,HIV-1 会抑制这些受体的信号,导致反应受到抑制,或者利用其信号为自身谋利。

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