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【聚焦】走进细胞自噬 [精华]

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tangdl2000

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Immunol Rev. 2011 Mar;240(1):92-104. doi: 10.1111/j.1600-065X.2010.00995.x.

Autophagy in immunity and cell-autonomous defense against intracellular microbes.
自噬与免疫以及微生物防御

Deretic V.

Department of Molecular Genetics and Microbiology, University of New Mexico Health Sciences Center, Albuquerque, NM, USA.

Abstract
Summary:? Autophagy was viewed until very recently primarily as a metabolic and intracellular biomass and organelle quality and quantity control pathway. It has now been recognized that autophagy represents a bona fide immunologic process with a wide array of roles in immunity. The immunologic functions of autophagy, as we understand them now, span both innate and adaptive immunity. They range from unique and sometimes highly specialized immunologic effectors and regulatory functions (referred to here as type I immunophagy) to generic homeostatic influence on immune cells (type II immunophagy), akin to the effects on survival and homeostasis of other cell types in the body. As a concept-building tool for understanding why and how autophagy is intertwined with immunity, it is useful to consider that the presently complex picture has emerged in increments, starting in part from the realization that autophagy acts as an evolutionarily ancient microbial clearance mechanism defending eukaryotic cells against intracellular pathogens. In this review, we build a stepwise model of how the core axis of autophagy as a cell-autonomous immune defense against microbes evolved into a complex but orderly web of intersections with innate and adaptive immunity processes. The connections between autophagy and conventional immunity systems include Toll-like receptors, Nod-like receptors, RIG-I-like receptors, damage-associated molecular patterns such as HMGB1, other known innate and adaptive immunity receptors and cytokines, sequestasome (p62)-like receptors that act as autophagy adapters, immunity-related GTPase IRGM, innate and adaptive functions of macrophages and dendritic cells, and differential effects on development and homeostasis of T- and B-lymphocyte subsets. The disease contexts covered here include tuberculosis, infections with human immunodeficiency virus and other viruses, Salmonella, Listeria, Shigella, Toxoplasma, and inflammatory disorders such as Crohn's disease and multiple sclerosis.

? 2011 John Wiley & Sons A/S.
PMID: 21349088

linelibrary.wiley.com+j.1600-065X.2010.00995.x.pdf(690.05k)

2011-02-28 22:26

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• 关于武汉肺炎疫情的一点个人见解

yuanruix

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先顶再下！感谢分享~

2011-03-01 00:02

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• [典型病例欣赏]40 观影识病肺部所见影像是什么？

dahaidenver

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Circulation. 2010 Sep 14;122(11 Suppl):S179-84.

Profound Cardioprotection With Chloramphenicol Succinate in the Swine Model of Myocardial
Ischemia-Reperfusion Injury琥珀氯霉素在猪心脏缺血/灌注模型中的极大的心脏保护作用

Cardiovascular Research Institute, Wayne State University School of Medicine, Detroit, MI 48201, USA.

Abstract

BACKGROUND: Emerging evidence suggests that "adaptive" induction of autophagy (the cellular process responsible for the degradation and recycling of proteins and organelles) may confer a cardioprotective phenotype and represent a novel strategy to limit ischemia-reperfusion injury. Our aim was to test this paradigm in a clinically relevant, large animal model of acute myocardial infarction. METHODS AND RESULTS: Anesthetized pigs underwent 45 minutes of coronary artery occlusion and 3 hours of reperfusion. In the first component of the study, pigs received chloramphenicol succinate (CAPS) (an agent that purportedly upregulates autophagy; 20 mg/kg) or saline at 10 minutes before ischemia. Infarct size was delineated by tetrazolium staining and expressed as a % of the at-risk myocardium. In separate animals, myocardial samples were harvested at baseline and 10 minutes following CAPS treatment and assayed (by immunoblotting) for 2 proteins involved in autophagosome formation: Beclin-1 and microtubule-associated protein light chain 3-II. To investigate whether the efficacy of CAPS was maintained with "delayed" treatment, additional pigs received CAPS (20 mg/kg) at 30 minutes after occlusion. Expression of Beclin-1 and microtubule-associated protein light chain 3-II, as well as infarct size, were assessed at end-reperfusion. CAPS was cardioprotective: infarct size was 25+/-5 and 41+/-4%, respectively, in the CAPS-pretreated and CAPS-delayed treatment groups versus 56+/-5% in saline controls (P<0.01 and P<0.05 versus control). Moreover, administration of CAPS was associated with increased expression of both proteins. CONCLUSIONS: Our results demonstrate attenuation of ischemia-reperfusion injury with CAPS and are consistent with the concept that induction of autophagy may provide a novel strategy to confer cardioprotection.

Profound Cardioprotection With Chloramphenicol.pdf(1086.78k)

2011-03-01 19:37

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• 怀疑病毒结膜传染，北大王广发：或因未带防护镜被感染

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tangdl2000

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Mol Cell. 2011 Feb 23. [Epub ahead of print]

Oncogenic Ras-Induced Expression of Noxa and Beclin-1 Promotes Autophagic Cell Death and Limits Clonogenic Survival.
RAS诱导自噬性死亡

Elgendy M, Sheridan C, Brumatti G, Martin SJ.

Molecular Cell Biology Laboratory, Department of Genetics, The Smurfit Institute, Trinity College, Dublin 2, Ireland.

Abstract
Deregulated oncogenes such as MYC and RAS are typically insufficient to transform cells on their own due to the activation of pathways that restrain proliferation. Previous studies have shown that oncogenic H-Ras can induce proliferative arrest or senescence, depending on the cellular context. Here, we show that deregulated H-Ras activity can also lead to caspase-independent cell death with features of autophagy. Ras-induced autophagy was associated with upregulation of the BH3-only protein Noxa as well as the autophagy regulator Beclin-1. Silencing of Noxa or Beclin-1 expression reduced Ras-induced autophagy and increased clonogenic survival. Ras-induced cell death was also inhibited by coexpression of Bcl-2 family members that inhibit Beclin-1 function. Ras-induced autophagy was associated with Noxa-mediated displacement of the Bcl-2 family member, Mcl-1, from Beclin-1. Thus, Ras-induced expression of Noxa and Beclin-1 promotes autophagic cell death, which represents a mechanism to limit the oncogenic potential of deregulated Ras signals.

Copyright ? 2011 Elsevier Inc. All rights reserved.
PMID: 21353614 [PubMed - as supplied by publisher]

123 ras.pdf(2262.52k)

2011-03-01 23:11

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• 现场 | 武汉新型肺炎：为何直到今天才引起更大注意？

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