天然免疫模式识别途径:胞外识别与胞内识别

天然免疫系统通常籍模式识别受体识别病原体相关分子模式。取决于感染的性质,模式识别受体通过细胞外 或细胞内途径识别病原体,并传导相应的信号,激活宿主防御应答,消灭入侵病原体。     

天然免疫识别的机制与途径

天然免疫系统的诱导性防御机制是由一系列模式识别受体对病原体的识别所启动的。这类受体识别一或几大组病原体所共有的分子模式，不但可发现入侵病原体的存在，而且能够识别其类型，并通过一系列信号途径控制各种免疫反应基因的表达而清除病原体。而天然免疫的抗肿瘤及部分抗病毒反应是一种对自身抗原的识别，所激发的信号途径发挥了免疫监视和防御功能。     

天然免疫识别的机制与途径

天然免疫系统的诱导性防御机制是由一系列模式识别受体对病原体的识别所启动的。这类受体识别一或几大组病原体所共有的分子模式 ,不但可发现入侵病原体的存在 ,而且能够识别其类型 ,并通过一系列信号途径控制各种免疫反应基因的表达而清除病原体。而天然免疫的抗肿瘤及部分抗病毒反应是一种对自身抗原的识别 ,所激发的信号途径发挥了免疫监视和防御功能。     

097 天然免疫识别的机制与途径

天然免疫系统的诱导性防御机制是由一系列模式识别受体对病原体的识别所启动的。这类受体识别一或几大组病原体所共有的分子模式，不但可发现入侵病原体的存在，而且能够识别其类型，并通过一系列信号途径控制各种免疫反应基因的表达而清除病原体。而天然免疫的抗肿瘤及部分抗病毒反应是一种对自身抗原的识别，所激发的信号途径发挥了免疫监视和防御功能。     

病毒感染的天然免疫识别机制

近年来提出的病原体相关分子模式（pathogen associated molecular pattern，PAMP）以及识别PAMP的模式识别受体（pattern recognition receptor，PRR）标志着天然免疫应答的研究进入新阶段。病毒感染的天然免疫应答依赖于宿主对病毒PAMP的识别，Toll样受体家族和胞内其他病毒模式识别受体介导的天然免疫机制也成为探讨的热点。本文着重概括一些病毒模式识别受体的功能和信号转导途径的研究近况。     

天然免疫系统的"分子模式识别作用"及其免疫生物学意义

天然免疫对配体的识别是“分子模式识别作用”,该作用不仅能绝对区分“自己”与“非已”,而且可区别无害“非已”和病原体相关“非已”,并通过抗原提呈和共刺激信号两个环节赋予获得性名单应答识别“自己”与“非已”的能力,筹划共诱导表达的一套不同的细胞因子得性免疫应答的类型。     

NOD1、NOD2:两个重要的天然免疫胞内识别受体

机体对微生物入侵的免疫炎症应答过程中模式识别受体(patternrecognitionreceptors,PRRs)是启动机体天然免疫应答机制的关键,主要在获得性免疫系统被活化之前发挥抗感染作用。NOD1和NOD2这两个蛋白分子作为一种新的胞内识别受体参与了细胞凋亡和核因子NF-κB的活化,并与一些炎症性疾病密切相关,在天然免疫中发挥了重要的作用。     

肽聚糖识别蛋白

天然免疫系统通过一系列高度保守的模式识别受体识别病原体相关分子模式.肽聚糖识别蛋白家族是重要的模式识别受体,从昆虫到人类均高度保守,可识别肽聚糖和含肽聚糖的细菌,在天然免疫和获得性免疫应答中发挥重要的识别和调节功能.     

甲型流感病毒天然免疫机制研究进展CSCD

流行性感冒病毒,简称流感病毒,属于正粘病毒科.流感病毒感染宿主后,急性高热、全身疼痛、显著乏力和呼吸道症状是其典型的临床症状.感染宿主后,可引起Toll样受体、RIG-Ⅰ样受体和NOD样受体等宿主模式识别受体介导的抗病毒信号通路的激活,诱导干扰素和IL-1,IL-18等细胞因子表达,起到抗病毒的作用.本文对这三类PRRs的作用机制进行阐述.     

天然免疫与获得性免疫的进化关系

免疫有天然免疫和获得性免疫两种类型,它们有不同的机制和起源.天然免疫可识别某些"非己”细胞或分子并加以清除;获得性免疫则对分子抗原表位进行识别,按抗原提呈细胞等有无协同信号(发育阶段/类型)而有所区别.两者有不同的生物学起源与意义;天然免疫源于防御入侵者的需求,获得性免疫则源于系统及个体自身发育中调节细胞发育的需求.两者嫁接性混合进化形成了复杂的可识别"自己/非己”的免疫系统,并留下了神奇的机制.     

Innate immune recognition: mechanisms and pathways

Summary: The innate immune system is an evolutionarily ancient form of host defense found in most multicellular organisms. Inducible responses of the innate immune system are triggered upon pathogen recognition by a set of pattern recognition receptors. These receptors recognize conserved molecular patterns shared by large groups of microorganisms. Recognition of these patterns allows the innate immune system not only to detect the presence of an infectious microbe, but also to determine the type of the infecting pathogen. Pattern recognition receptors activate conserved host defense signaling pathways that control the expression of a variety of immune response genes.     

Innate immunity: Antigen recognition: Web Alert

A selection of World Wide Web sites relevant to papers published in this issue of Current Opinion in Immunology.     

Innate immunity: cells, receptors, and signaling pathways

Essential differences between the innate and acquired branches of immunity are described. These differences concern the detection system (receptors and pathogen structures) and the cells engaged in both systems as well as the effectory mechanisms. In contrast to those of the acquired system, receptors of the innate system, which developed during evolution, recognize unchanged structures on large groups of pathogens (e.g. lipopolysaccharide in Gram-negative bacteria). Two lineages, natural killer (NK) and dendritic cells (DCs), play important roles in the innate system. Phenotypic and functional differentiation is observed among NKs and DCs, so each of their sublineages plays a different role in the innate system. Every lineage of cells of the innate immune system express different stimulatory and sometimes also inhibitory receptors on their surfaces (e.g. NK cells). Among the stimulatory are Toll-like receptors (TLRs), mannose and scavenger receptors, and the stimulatory receptors of NK cells. All TLRs show similarity in structure and in the kind of molecules involved in intracellular signaling. The immune reactions of the innate system involve cytokine-dependent resistance of cells against infection with pathogen, production of cytokines (tumor necrosis factor, interferons, interleukins, chemokines) and MHC-independent killing. Although these reactions protect the host from invasion by microorganisms, they can also be responsible for significant tissue damage or may stimulate the development of autoimmunity. Therefore innate immunity must be under rigorous control. The possible regulatory mechanisms of innate immunity are discussed.     

Innate immunity in self and infectious nonself recognition

Response to: Ameratunga R, Woon S-T, Gillis D et al. Challenges in diagnosis of CVID. Expert Rev. Clin. Immunol. 10(2), 000–000 (2014).     

Innate immunity turned inside-out: antimicrobial defense by phagocyte extracellular traps

The formation of extracellular traps (ETs) by phagocytic cells has been recognized as a novel and important mechanism of the host innate immune response against infections. ETs are formed by different host immune cells such as neutrophils, mast cells, and eosinophils after stimulation with mitogens, cytokines, or pathogens themselves, in a process dependent upon induction of a reactive-oxygen-species-mediated signaling cascade. ETs consist of nuclear or mitochondrial DNA as a backbone with embedded antimicrobial peptides, histones, and cell-specific proteases and thereby provide a matrix to entrap and kill microbes and to induce the contact system. This review summarizes the latest research on ETs and their role in innate immunity and host innate defense. Attention is also given to mechanisms by which certain leading bacterial pathogens have evolved to avoid entrapment and killing in these specialized structures.     

Innate immunity signaling pathways: links between immunonutrition and responses to sepsis

Septic infections in patients treated in intensive care units show the highest mortality rates. Despite advances in treatment methods, there is still no therapy available to efficiently reduce the excessive inflammatory response, which can increase the risk of multiple organ failure. One of the ways to discover new, more efficient treatment methods involves regulating the mechanisms of inflammatory response to a massive infection. Toll-like receptors (TLRs) that recognize pathogen-associated molecular patterns play a significant role in innate antibacterial and inflammatory responses. The regulatory impact of immunonutrition on TLR expression in septic patients seems to be a promising research direction. This paper presents the main mechanisms for the innate immune response to lipopolysaccharide, based on the research results for both TLR-dependent and independent signaling pathways. Special emphasis was put on the research results for the TLR-dependent immune response and the anti-bacterial/anti-inflammatory response after applying immunonutrition with increased concentrations of glutamine and unsaturated fatty acids.