Killing HIV-infected resting central memory CD4 T cells by targeting inhibitor of apoptosis proteins-inhibited autophagy

Dysfunction of CD4 + T cells by HIV infection can cause serious immune defects. Recently, Campbell and colleagues described an intriguing and simple therapeutic method for HIV-infected resting central memory CD4 + T cells (HIV-T CM ), dependently on inhibitor of apoptosis (IAP) family proteins-targe...

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Main Authors: Gang Zhang, Xing Huang
Format: Article
Language:English
Published: SAGE Publishing 2021-02-01
Series:Antiviral Chemistry & Chemotherapy
Online Access:https://doi.org/10.1177/2040206620980888
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spelling doaj-e443f95479f8473d80b5ffa194ccc0af2021-02-10T04:04:58ZengSAGE PublishingAntiviral Chemistry & Chemotherapy2040-20662021-02-012910.1177/2040206620980888Killing HIV-infected resting central memory CD4 T cells by targeting inhibitor of apoptosis proteins-inhibited autophagyGang ZhangXing HuangDysfunction of CD4 + T cells by HIV infection can cause serious immune defects. Recently, Campbell and colleagues described an intriguing and simple therapeutic method for HIV-infected resting central memory CD4 + T cells (HIV-T CM ), dependently on inhibitor of apoptosis (IAP) family proteins-targeted and second mitochondria-derived activator of caspases (SMAC) mimetics-mediated apoptosis, which is only triggered in HIV-T CM and not uninfected ones. Autophagy induction and subsequent formation of a ripoptosome-like death signaling complex were observed after such treatment, which may partially explain the potential mechanism. However, the direct intracellular inhibitory effects of IAPs on autophagy, as well as the critical roles of autophagy in activating extracellular anti-infection immune responses, warrant further investigation. Thus, this pointer aims to provide potential alternative mechanisms and to suggest important avenues for follow-up study.https://doi.org/10.1177/2040206620980888
collection DOAJ
language English
format Article
sources DOAJ
author Gang Zhang
Xing Huang
spellingShingle Gang Zhang
Xing Huang
Killing HIV-infected resting central memory CD4 T cells by targeting inhibitor of apoptosis proteins-inhibited autophagy
Antiviral Chemistry & Chemotherapy
author_facet Gang Zhang
Xing Huang
author_sort Gang Zhang
title Killing HIV-infected resting central memory CD4 T cells by targeting inhibitor of apoptosis proteins-inhibited autophagy
title_short Killing HIV-infected resting central memory CD4 T cells by targeting inhibitor of apoptosis proteins-inhibited autophagy
title_full Killing HIV-infected resting central memory CD4 T cells by targeting inhibitor of apoptosis proteins-inhibited autophagy
title_fullStr Killing HIV-infected resting central memory CD4 T cells by targeting inhibitor of apoptosis proteins-inhibited autophagy
title_full_unstemmed Killing HIV-infected resting central memory CD4 T cells by targeting inhibitor of apoptosis proteins-inhibited autophagy
title_sort killing hiv-infected resting central memory cd4 t cells by targeting inhibitor of apoptosis proteins-inhibited autophagy
publisher SAGE Publishing
series Antiviral Chemistry & Chemotherapy
issn 2040-2066
publishDate 2021-02-01
description Dysfunction of CD4 + T cells by HIV infection can cause serious immune defects. Recently, Campbell and colleagues described an intriguing and simple therapeutic method for HIV-infected resting central memory CD4 + T cells (HIV-T CM ), dependently on inhibitor of apoptosis (IAP) family proteins-targeted and second mitochondria-derived activator of caspases (SMAC) mimetics-mediated apoptosis, which is only triggered in HIV-T CM and not uninfected ones. Autophagy induction and subsequent formation of a ripoptosome-like death signaling complex were observed after such treatment, which may partially explain the potential mechanism. However, the direct intracellular inhibitory effects of IAPs on autophagy, as well as the critical roles of autophagy in activating extracellular anti-infection immune responses, warrant further investigation. Thus, this pointer aims to provide potential alternative mechanisms and to suggest important avenues for follow-up study.
url https://doi.org/10.1177/2040206620980888
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