NOD 样受体在免疫耐受中的作用

正Toll样受体(Toll-like receptors,TLR)和NOD样受体(Nucleotide binding oligomerization domain-like receptors,NLR)为代表的模式识别受体(Pattern recognition receptors,PRR)在固有免疫等领域发挥着重要作用,其中NLR作为一类胞内模式识别受体在免疫耐受领域也得到越来越多的关注。本文对NLR     

PPARα在心血管疾病中作用机制的研究进展

过氧化物酶体增殖物激活受体(peroxisome proliferator-activated receptors,PPARs)有3种类型:过氧化物酶体增殖物激活受体α(peroxisome proliferator-activated receptorsα,PPARα),过氧化物酶体增殖物激活受体β/δ(peroxi...     

胆碱M受体的研究进展

乙酰胆碱(Acetylcholine,Ach)是胆碱能神经的递质,与Ach结合的受体称为Ach受体。按照受体结构和对药物反应的不同,被毒蕈碱激活的Ach受体称为毒蕈碱型Ach受体(Muscarinicacetylcholine receptors,M受体);被烟碱激动的Ach受体称为烟碱型Ach受体(Nicotinic acetyl-choline receptors,N受体)。在外周神经系统可参与调节平滑肌收缩、腺体分泌、心率和心肌收缩力;在中枢神经系统,M受体与运动、体温、心血管功能、学习和记忆的调节有关。本文就M受体的结构、作用和信号传导过程作一简要综述。     

大麻素受体激活调控牙周炎症和骨改建促进牙周组织愈合

背景:大麻素受体通过与配体结合,调控牙周炎的炎症和骨量,促进牙周组织的愈合,在临床上牙周炎的预防和治疗方面具有重要意义。目的:综述大麻素受体与牙周炎的关系,主要为大麻素Ⅰ型(CB1)受体、大麻素Ⅱ型(CB2)受体与炎症和牙槽骨骨改建的关系,以及涉及的常见细胞信号传导通路,为牙周炎预防和治疗及其在临床其他领域的应用提供思路。方法:检索PubMed、万方数据库、CNKI中国期刊全文数据库1985年7月至2022年7月收录的相关文献。英文检索词为“cannabinoids receptor,CB1 receptor and periodontitis,CB2 receptor and periodontitis,CB1 receptors and bone remodeling,CB2 receptors and bone remodeling,CB1 receptors and signaling pathways,CB2 receptors and signaling pathways”,中文检索词为“大麻素受体,CB1受体和牙周炎,CB2受体和牙周炎,CB1受体和骨改建,CB2受体和骨...     

病毒相关Toll样受体研究进展

Toll样受体(Toll like receptors,TLR)是近来发现的固有性免疫系统中的细胞跨膜受体及病原模式识别受体之一,在对病毒的识别与免疫应答作用中起着重要的用。本文简要综述了病毒相关Toll样受体中TLR2、3、4、7、8、9的研究进展。     

视黄酸诱导基因-Ⅰ样受体与抗病毒固有免疫的研究进展

机体的固有免疫应答在抵抗病毒感染方面发挥着重要作用,该应答的前提是参与固有免疫的细胞通过模式识别受体(Pattern recognition receptors,PRRs)对病毒的病原体相关分子模式(Pathogen-asso-ciated molecular patterns,PAMPs)进行识别,发生受体配体反应,进而诱导干扰素和促炎症细胞因子的表     

Toll样受体与自身免疫性肝病

Toll样受体(Toll like receptors,TLRs)是近些年来发现的一类新的细胞表面信号传导跨膜受体,能够识别作为配体的病原相关的分子模式(Pathogen-associated molecular patterns,PAMPs),是人体固有免疫和适应性免疫的桥梁[1].     

Toll样受体在人乳头瘤病毒感染致宫颈癌中的作用

高危型人乳头瘤病毒(high-risk human papillomavirus,HR-HPV)持续感染是宫颈癌发生的明确病因,但并非所有HR-HPV感染都会导致宫颈癌,说明多种因素参与调节HR-HPV的致病性。Toll样受体(Toll-like receptors,TLRs)是一类模式识别受体,能特异性识别病原体相关...     

第一组代谢型谷氨酸受体在外周痛信号产生中的作用

谷氨酸是脑内最重要的兴奋性递质 ,除参与快速的兴奋性突触传递外 ,还与突触前递质释放、突触传递的长时程增强和长时程抑制、学习和记忆过程、突触发育的可塑性等正常生理功能密切相关。谷氨酸过量时还具有神经毒作用 ,可导致神经元死亡。谷氨酸受体分为两类 :(1)离子型谷氨酸受体 (ionotrop-ic glutam ate receptors,i Glu Rs) ,属于配体门控离子通道 ,包括 NMDA、AMPA和 KA三种亚型 ,均以异源性蛋白的多聚体形式存在 [1 ] ;(2 )代谢型谷氨酸受体 (m etabotropic gluta-mate receptors,m Glu Rs) ,是一组新型的 G-蛋白偶联受体。m …     

蛋白酶激活受体在炎症中的作用

蛋白酶激活受体(Proteinase-activated receptors,PARs)是G蛋白偶联受体家族的一员,介导跨膜信号转导并调节 细胞的功能。它被激活后参与许多疾病的发生和发展过程,尤其在炎症反应中所起的作用受到人们越来越多的关注。     

NOD-like receptors (NLRs): bona fide intracellular microbial sensors

The nucleotide-binding oligomerization domain (NOD)-like receptor (NLR) (nucleotide-binding domain leucine-rich repeat containing) family of proteins has been demonstrated to function as regulators of innate immune response against microbial pathogens. Stimulation of NOD1 and NOD2, two prototypic NLRs, results in the activation of MAPK and NF-kappaB. On the other hand, a different set of NLRs induces caspase-1 activation through the assembly of an inflammasome. This review discusses recent findings regarding the signaling pathways utilized by NLR proteins in the control of caspase-1 and NF-kappaB activation, as well as the nonredundant role of NLRs in pathogen clearance. The review also covers advances regarding the cellular localization of these proteins and the implications this may have on pathogen sensing and signal transduction.     

Infectious non-self recognition in invertebrates: lessons from Drosophila and other insect models

The vertebrate innate immune system recognizes infectious non-self by employing a set of germline-encoded receptors such as nucleotide-binding oligomerisation domain proteins (NODs) or Toll-like receptors (TLRs). These proteins are involved in the recognition of various microbial-derived molecules, including lipopolysaccharide (LPS), peptidoglycan (PGN) and beta1,3-glucan. Drosophila Toll receptors are not directly dedicated to non-self recognition and insect NOD orthologues have not yet been identified. Studies started more than 20 years ago and conducted on different insect models have identified other receptors on which invertebrate innate systems rely to sense invading microorganisms.     

NOD2-associated diseases: Bridging innate immunity and autoinflammation

NOD2 is an intracellular microbial sensor of the innate immune system that can act as a potent activator and regulator of inflammation. Mutations in the gene encoding NOD2 in humans have been associated with Crohn's disease (CD), Blau syndrome (BS), and early onset sarcoidosis (EOS). These diseases have in common features of dysregulated inflammation, but have very distinct phenotypes, which have been hypothesized to result from either loss-of-function (CD) or gain-of-function (BS/EOS) mutations. Here we describe an infant with early onset sarcoidosis who presented with systemic inflammation and disseminated granulomatous disease, including the triad of granulomatous arthritis, uveitis and dermatitis, as well as unusual gastrointestinal tract granulomas. The patient had a susceptibility polymorphism of NOD2 previously described in CD, but not in BS or EOS. We discuss the complex role of NOD2 in innate immunity to microbes and the clinical consequences of disturbances in this system.     

The ever-expanding function of NOD2: autophagy, viral recognition, and T cell activation

The identification of several families of innate pattern recognition receptors has greatly enhanced our understanding of the host innate immune response against a variety of pathogens. One such family of innate receptors is the nucleotide-binding domain and leucine rich repeat containing receptors (NLRs). NOD2 has been characterized as a cytosolic sensor of bacteria peptidoglycan (PGN). For almost 10 years, NOD2 was assigned with the function of mediating the RICK- and nuclear factor-κB induced proinflammatory response triggered by PGN. Recent studies have extended the biological activity of NOD2 to include the induction of autophagy and antiviral responses, as well as mediating direct T cell activation. Here, we highlight and discuss these new findings in the context of immune activation and pathogen detection.     

Molecular diversity at the plant-pathogen interface

Plants have evolved a robust innate immune system that exhibits striking similarities as well as significant differences with various metazoan innate immune systems. For example, plants are capable of perceiving pathogen-associated molecular patterns through pattern recognition receptors that bear structural similarities to animal Toll-like receptors. In addition, plants have evolved a second surveillance system based on cytoplasmic "NB-LRR" proteins (nucleotide-binding, leucine-rich repeat) that are structurally similar to animal nucleotide-binding and oligomerization domain (NOD)-like receptors. Plant NB-LRR proteins do not detect PAMPs; rather, they perceive effector proteins that pathogens secrete into plant cells to promote virulence. This review summarizes the current state of knowledge about the molecular functionality and evolution of these immune surveillance genes.     

NOD受体-细胞内的模式识别受体家族

真核生物通过先天免疫和获得性免疫识别和清除入侵的病原微生物。同获得性免疫相比,先天免疫在病原体入侵后能迅速被激活,形成了防御病原体入侵的第一道防线。先天免疫系统是通过特殊的模式识别受体(pattern-recognition receptors,PRRs)感知病原体关联的分子模式(pathogen-ass     

NOD1和NOD2与炎性肠病

NOD1和NOD2蛋白是一类新型胞浆内模式识别受体,在宿主固有免疫和自噬过程中起着关键的作用,对维持肠道微生态和黏膜屏障作用至关重要,研究表明NOD1和NOD2基因多态性和表达异常与炎性肠病的发生密切有关.     

参与免疫及炎症反应调控的胞浆蛋白NODs

Nucleotide- binding oligomerization domain (NOD) proteins are members of a growing family of cytosolic factors related to the apoptosis regulator Apaf-1 and a class of plant disease resistance proteins. NOD proteins have been implicated in the induction of NF-κB activity and in the activation of caspases. Biochemical evidence has unraveled the role of NOD1 and NOD2 as intraceUular sensors of bacterial peptidoglycan. Notably, genetic variation in the genes encoding the NOD proteins NOD2, cryopyrin and C Ⅱ TA inhmnans is associated with inflammatory disease or increased susceptibility to bacterial infections. NOD proteins may be involved in the recognition of microorganisms and regulation of inflammatory responses.     

Modification of the structure of peptidoglycan is a strategy to avoid detection by nucleotide-binding oligomerization domain protein 1

Nucleotide-binding oligomerization domain (NOD) protein 1 (NOD1) and NOD2 are pathogen recognition receptors that sense breakdown products of peptidoglycan (PGN) (muropeptides). It is shown that a number of these muropeptides can induce tumor necrosis factor alpha (TNF-alpha) gene expression without significant TNF-alpha translation. This translation block is lifted when the muropeptides are coincubated with lipopolysaccharide (LPS), thereby accounting for an apparently synergistic effect of the muropeptides with LPS on TNF-alpha protein production. The compounds that induced synergistic effects were also able to activate NF-kappaB in a NOD1- or NOD2-dependent manner, implicating these proteins in synergistic TNF-alpha secretion. It was found that a diaminopimelic acid (DAP)-containing muramyl tetrapeptide could activate NF-kappaB in a NOD1-dependent manner, demonstrating that an exposed DAP is not essential for NOD1 sensing. The activity was lost when the alpha-carboxylic acid of iso-glutamic acid was modified as an amide. However, agonists of NOD2, such as muramyl dipeptide and lysine-containing muramyl tripeptides, were not affected by amidation of the alpha-carboxylic acid of iso-glutamic acid. Many pathogens modify the alpha-carboxylic acid of iso-glutamic acid of PGN, and thus it appears this is a strategy to avoid recognition by the host innate immune system. This type of immune evasion is in particular relevant for NOD1.