Center for Experimental and Molecular Medicine and Center for Infection and Immunity Amsterdam, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.
Curr Opin HIV AIDS. 2011 Sep;6(5):348-52. doi: 10.1097/COH.0b013e328349a2d1.
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.
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.
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.
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。
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。
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。
