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炎症小体在对抗微生物感染中的作用 被引量:16

Function of Inflammasomes in Anti-microbial Infections
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摘要 炎症小体(inflammasomes)是由胞浆内模式识别受体(PRRs)参与组装的多蛋白复合物,是天然免疫系统的重要组成部分。炎症小体能够识别病原相关分子模式(PAMPs)或者宿主来源的危险信号分子(DAMPs),招募和激活促炎症蛋白酶Caspase-1。活化的Caspase-1切割IL-1β和IL-18的前体,产生相应的成熟细胞因子。炎症小体的活化还能够诱导细胞的炎症坏死(pyroptosis)。目前已经确定多种炎症小体参与了针对多种病原体的宿主防御反应,病原体也已经进化出多种相应的机制来抑制炎症小体的活化。该文总结了炎症小体在抗感染免疫研究领域的最新进展,重点讨论了炎症小体对细菌、病毒、真菌和寄生虫的识别,以及炎症小体的活化在宿主抗感染过程中所发挥的作用。 As an important component of the innate immune system, inflammasomes are multi-protein complexes in the cytoplasm scaffolded by intracellular pattern recognition receptors (PRRs). Inflammasomes can be activated by sensing pathogen-associated molecular patterns (PAMPs) or host-derived danger signals, resulting in the recruitment and activation of the cysteine protease caspase-1. Activated caspase-1 is critical in the proteolytic processing of pro-interleukin- 1 β (pro-IL- 1β) and pro-IL- 18 into their mature cytokine forms, respectively. In addition, caspase-1 mediated cell death, pyroptosis, has been revealed to be an efficient mechanism for pathogen clearance. To date, multiple inflammasomes have been shown to be involved in the elimination of a growing number of microbial pathogens. In turn, pathogens have also evolved a plethora of strategies to abrogate the inflammasomes mediated immune responses. In this review we retrospect our new knowledge about inflammasomemediated recognition of microbial pathogens, including that of bacterial, viral, fungal and protozoal, as well as the favorable or unfavorable effects of inflammasomes activation in host defense.
出处 《中国细胞生物学学报》 CAS CSCD 2011年第12期1301-1315,共15页 Chinese Journal of Cell Biology
基金 中国科学院百人计划(No.2010A1119) 中国科学院上海生命科学研究院博士后研究项目(No.2011KIP513) 国家自然科学基金(No.91029707 No.31170868) 上海市自然科学基金(No.11ZR1442600) 诺和诺德-中科院联合研究基金 中国博士后科学基金面上项目(No.20110490752) 国家自然科学基金青年科学基金(No.31100622)资助项目~~
关键词 天然免疫 炎症小体 炎症 感染 innate immunity inflammasomes inflammation infection
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  • 1Medzhitov R. Origin and physiological roles of inflammation. Nature 2008; 454(7203): 428-35.
  • 2Akira S, Uematsu S, Takeuchi O. Pathogen recognition and innate immunity. Cell 2006; 124(4): 783-801.
  • 3Takeuchi O, Akira S. Pattern recognition receptors and inflammation. Cell 2010; 140(6): 805-20.
  • 4Tschopp J, Martinon F, Bums K. NALPs: A novel protein family involved in inflammation. Nat Rev Mol Cell Biol 2003; 4(2): 95-104.
  • 5Allen IC, Moore CB, Schneider M, Lei Y, Davis BK, Scull MA, et al. NLRX1 protein attenuates inflammatory responses to infection by interfering with the RIG-I-MAVS and TRAF6-NFkappaB signaling pathways. Immunity 2011; 34(6): 854-65.
  • 6lnohara N, Ogura Y, Fontalba A, Gutierrez O, Pons F, Crespo J, et aL Host recognition of bacterial muramyl dipeptide mediated through NOD2. Implications for Crohn's disease. J Biol Chem 2003; 278(8): 5509-12.
  • 7Girardin SE, Boneca IG, Carneiro LA, Antignac A, Jehanno M, Viala J, et al. Nodl detects a unique muropeptide from gramnegative bacterial peptidoglycan. Science 2003; 300(5625): 1584-7.
  • 8Park JH, Kim YG, McDonald C, Kanneganti TD, Hasegawa M, Body-Malapel M, et al. RICK/RIP2 mediates innate immune responses induced through Nodl and Nod2 but not TLRs. J Irnmuno12007; 178(4): 2380-6.
  • 9Abbott DW, Yang Y, Hutti JE, Madhavarapu S, Kelliher MA, Cantley LC. Coordinated regulation of Toll-like receptor and NOD2 signaling by K63-1inked polyubiquitin chains. Mol Cell Bio12007; 27(17): 6012-25.
  • 10Schroder K, Tschopp J. The inftammasomes. Cell 2010; 140(6): 821-32.

同被引文献146

  • 1蔡娟,都建,汪学龙,沈继龙.重组弓形虫14-3-3抗原用于弓形虫血清抗体的检测[J].安徽医科大学学报,2005,40(2):147-149. 被引量:4
  • 2赵英男,左云飞.凋亡相关的斑点样蛋白ASC[J].生命的化学,2006,26(3):239-241. 被引量:4
  • 3Miller C M , Houller N R, Ikin K J , et al. The immunohiology ofthe imiatt, r<*sponse to Toxoplasma gondii [ J ] Int J Trarasitol,2009,39( 1 ) :23 -39.
  • 4Fukata M, Vamadevan A S, Ahreu M T. Toll-like reoeptors(TLHs) and Nod-Iikt? receptors ( NLRs) in inflammatory disorders[J]. Semin Immunol, 2009,21 (4) :242 -53.
  • 5Lanikanfi M,Kanneganti T I). Nir[>3 : An immune sensor ol' cellularstress and infeclion[J]. Int J Biochem Cell liiol, 2010 ,42 (6 ):792 -5.
  • 6Ichinohe I\Pang I K,Iwasaki A. Influenza virus activates inf];un-masomes via its intracellular M2 ion channel [ J ]. Nat Immunol,2010,11(5):404 -10.
  • 7Munoz-Planillo R, Franchi L,Miller L S,et al. A critical role forhemolysins and bacterial lipoproteins in Staphylococcus aureus-'m-duced activation of the Nlrp3 inflammasome [ J ]. J Immunol,2009,183(6) : 3942 -8.
  • 8Hise A G,Tomalka J, Ganesan S, et al. An essential role for theNLRP3 inflammasome in host defense against the human fungalpathogen Candida albicans [J]. Cell Host Microbe,2009, 5(5):487 -97.
  • 9Harder J,Franchi L, Mufloz-Planillo R,et al. Activation of the Nl-rp3 inflammasome by Streptococcus pyogenes requires streptolysin Oand NF-kappa B activation but proceeds independently of TLR sig-naling and P2X7 receptor [ J]. J Immunol,2009,183(9) :5823-9.
  • 10Duncan J A,Gao X,Huang M T,et al. Neisseria gonorrhoeae acti-vates the proteinase cathepsin B to mediate the signaling activitiesof the NLRP3 and ASC-containing inflammasome [ J ]. J Immunol,2009, 182(10) :6460-9.

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