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YU Yinghua, XU Zhimeng, ZENG Hao, NI Rongxing, LI Ping. Advances in the study of relationship between Caspases and innate immunity[J]. Journal of China Pharmaceutical University, 2019, 50(5): 622-630. DOI: 10.11665/j.issn.1000-5048.20190517
Citation: YU Yinghua, XU Zhimeng, ZENG Hao, NI Rongxing, LI Ping. Advances in the study of relationship between Caspases and innate immunity[J]. Journal of China Pharmaceutical University, 2019, 50(5): 622-630. DOI: 10.11665/j.issn.1000-5048.20190517

Advances in the study of relationship between Caspases and innate immunity

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  • Caspases are a group of structurally related cysteine proteases present in cytosol. One of their important common points is that the active sites contain cysteine and can specifically break the peptide bonds after the aspartic acid residues. Caspases are broadly divided into two groups based on their functions, including inflammatory Caspases and apoptotic Caspases. Inflammatory Caspases include Caspase-1, Caspase-4, Caspase-5, Caspase-11 and Caspase-12, which play important roles in the process of innate immune defense. Unlike inflammatory Caspases, apoptotic Caspases(2/3/6/7/8/910)initiate and execute an immunologically silent form of programmed cell death known as apoptosis. However, ongoing investigations have uncovered essential functions of Caspase-8 in the regulation of immunity in cells and organisms. Accumulated studies have shown that Caspases play important roles in the occurrence and development of various immunity-related diseases. In order to comprehensively elucidate the relationship between Caspases and innate immunity, and to provide some scientific basis and theoretical reference for the treatment of various diseases, this article reviews the regulation of activity and inflammation mechanism of innate immunity-related Caspase-1/4/5/11/8/12.
  • [1]
    Takanori K,Daniel AM.The role of inflammasomes in kidney disease[J].Nat Rev Nephrol,2019.doi: 10.1038/s41581-019-0158-z.
    [2]
    Martinon F,Burns K,Tschopp J.The inflammasome:a molecular platform triggering activation of inflammatory caspases and processing of proIL-beta[J].Molecular Cell,2002,10(2):417-426.
    [3]
    Yi YS.Caspase-11 non-canonical inflammasome:a critical sensor of intracellular lipopolysaccharide in macrophage-mediated inflammatory responses[J].Immunology,2017,152(2):207-217.
    [4]
    Man SM,Kanneganti TD.Converging roles of Caspases in inflammasome activation,cell death and innate immunity[J].Nat Rev Immunol,2016,16(1):7-21.
    [5]
    Gurung P,Kanneganti TD.Novel Roles for Caspase-8 in IL-1β and Inflammasome Regulation[J].Am J Pathol,2015,85(1):17-25.
    [6]
    Chen HH,Ning XH,Jiang ZF.Caspases control antiviral innate immunity[J].Cell Mol Immunol,2017,14(9):736-747.
    [7]
    Winsor N,Krustev C,Bruce J,et al.Canonical and non-canonical inflammasomes in intestinal epithelial cells[J].Cell Microbiol,2019.doi: 10.1111/cmi.13079.
    [8]
    He WT,Wan HQ,Hu LC,et al.Gasdermin D is an executor of pyroptosis and required for interleukin-1β secretion[J].Cell Res,2015,25(12):1285-1298.
    [9]
    Mitchell PS,Sandstrom A,Vance RE,et al.The NLRP1 inflammasome:new mechanistic insights and unresolved mysteries[J].Curr Opin Immunol,2019,60:37-45.
    [10]
    Minkiewicz J,Vaccari JPD,Keane RW.Human astrocytes express a novel NLRP2 inflammasome[J].Glia,2013,61(7):1113-1121.
    [11]
    Mangan MSJ, Olhava EJ, Roush WR. Targeting the NLRP3 inflammasome in inflammatory diseases[J].Nat Rev Drug Disco,2018,17(8):588-606.
    [12]
    Zhao Y, Shao F. The NAIP-NLRC4 inflammasome in innate immune detection of bacterial flagellin and type III secretion apparatus[J].Nat Rev,2015,265(1):85-102.
    [13]
    Hu ZH, Zhou Q, Zhang CL, et al. Structural and biochemical basis for induced self-propagation of NLRC4[J].Science,2015,350(6259):399-404.
    [14]
    Levy M,Thaiss CA,Zeevi D,et al.Microbiota-modulated metabolites shape the intestinal microenvironment by regulating NLRP6 inflammasome signaling[J].Cell,2015,163(6):1428-1443.
    [15]
    Hara H,Seregin SS,Yang DH,et al.The NLRP6 inflammasome recognizes lipoteichoic acid and regulates gram-positive pathogen infection[J].Cell,2018,175(6):1651-1664.
    [16]
    Zhu S,Ding SY,Wang PH,et al.Nlrp9b inflammasome restricts rotavirus infection in intestinal epithelial cells[J].Nature,2017,546(7660):667-670.
    [17]
    Park YH,Wood G,Kastner DL,et al.Pyrin inflammasome activation and RhoA signaling in the autoinflammatory diseases FMF and HIDS[J].Nat Immunol,2016,17(8):914-921.
    [18]
    Xu H,Yang JL,Gao WQ,et al.Innate immune sensing of bacterial modifications of Rho GTPases by the Pyrin inflammasome[J].Nature,2014,513(7517):237-241.
    [19]
    Lugrin J,Martinon F.The AIM2 inflammasome:Sensor of pathogens and cellular perturbations[J].Immunol Rev,2018,281(1):99-114.
    [20]
    Kerur N, Veettil MV, Sharma-Walia N, et al. IFI16 acts as a nuclear pathogen sensor to induce the inflammasome in response to Kaposi Sarcoma-associated herpesvirus infection[J].Cell Host Microbe,2011,9(5):363-375.
    [21]
    Elinav E,Strowig T,Henao-Mejia J,et al.Regulation of the antimicrobial response by NLR proteins[J].Immunity,2011,34(5):665-679.
    [22]
    Cordero MD,Williams MR,Ryffel B.AMP-activated protein kinase regulation of the NLRP3 inflammasome during aging[J].Trends Endocrin Met,2018,29(1):8-17.
    [23]
    Gong T,Yang YQ,Jin TC,et al.Orchestration of NLRP3 inflammasome activation by ion fluxes[J].Trends Immunol,2018,39(5):393-406.
    [24]
    He Y,Zeng MY,YangD,et al.NEK7 is an essential mediator of NLRP3 activation downstream of potassium efflux[J].Nature,2016,530(7590):354-357.
    [25]
    Liu QY,Zhang DY,Hu DY,et al.The role of mitochondria in NLRP3 inflammasome activation[J].Mol Immunol,2018,469:115-124.
    [26]
    Gaidt MM,Ebert TS,Chauhan D,et al.The DNA inflammasome in human myeloid cells is initiated by a STING-cell death program upstream of NLRP3[J].Cell,2017,171(5):1110-1124.
    [27]
    He Y,Hara H,Núñez G.Mechanism and regulation of NLRP3 inflammasome activation[J].Trends Biochem Sci,2016,41(12):S0968000416301487.
    [28]
    Levinsohn JL,Newman ZL,Hellmich KA,et al.Anthrax lethal factor cleavage of Nlrp1 is required for activation of the inflammasome[J].PLoS Pathog,2012,8(3):e002638.
    [29]
    Sandstrom A,Mitchell PS,Goers L,et al.Functional degradation:A mechanism of NLRP1 inflammasome activation by diverse pathogen enzymes[J].Science,2019,364(6435):eaau1330.
    [30]
    Chui AJ,Okondo MC,Rao SD,et al.N-terminal degradation activates the NLRP1B inflammasome[J].Science,2019,364(6435):82-85.
    [31]
    Rathinam VAK,Zhao Y,Shao F.Innate immunity to intracellular LPS[J].Nat Immunol,2019,20:527-533.
    [32]
    Liu X,Zhang ZB,Ruan JB,et al.Inflammasome-activated gasdermin D causes pyroptosis by forming membrane pores[J].Nature,2016,535(7610):153-158.
    [33]
    Vanaja SK,Russo AJ,Behl B,et al.Bacterial outer membrane vesicles mediate cytosolic localization of LPS and Caspase-11 activation[J].Cell,2016,165(5):1106-1119.
    [34]
    Kayagaki N,Stowe IB,Lee BL,et al.Caspase-11 cleaves gasdermin D for non-canonical inflammasome signalling[J].Nature,2015,526(7575):666-671.
    [35]
    Ding JJ,Shao F.Snapshot:the noncanonical inflammasome[J].Cell,2017,168(3):544-544.
    [36]
    Ruehl S,Broz P.Caspase-11 activates a canonical NLRP3 inflammasome by promoting K+ efflux[J].Eur J Immunol,2015,45(10):2927-2936.
    [37]
    Zanoni I,Tan YH,Di Gioia M,et al.An endogenous Caspase-11 ligand elicits interleukin-1 release from living dendritic cells[J].Science,2016,352(6290):1232-1236.
    [38]
    Chu LH,Indramohan M,Ratsimandresy RA,et al.The oxidized phospholipid oxPAPC protects from septic shock by targeting the non-canonical inflammasome in macrophages[J].Nat Commun,2018,9(1):996.
    [39]
    DeLaney AA,Berry CT,Christian DA,et al.Caspase-8 promotes c-Rel-dependent inflammatory cytokine expression and resistance against Toxoplasma gondii[J].Proc Natl Acad Sci U S A,2019,116(24):11926-11935.
    [40]
    Orning P,Weng D,Starheim K,et al.Pathogen blockade of TAK1 triggers Caspase-8-dependent cleavage of gasdermin D and cell death[J].Science,2018,362(6418):1064-1069.
    [41]
    Sarhan J,Liu BC,Muendlein HI,et al.Caspase-8 induces cleavage of gasdermin D to elicit pyroptosis during Yersinia infection[J].Proc Natl Acad Sci U S A,2018,115(46):E10888-E10897.
    [42]
    Kang TB,Yang SH,Toth B,et al.Caspase-8 blocks kinase RIPK3-mediated activation of the NLRP3 inflammasome[J].Immunity,2013,38(1):27-40.
    [43]
    Tummers B,Green DR.Caspase-8:regulating life and death[J].Immunol Rev,2017,77(1):76-89.
    [44]
    Maelfait J,Vercammen E,Janssens S,et al.Stimulation of Toll-like receptor 3 and 4 induces interleukin-1β maturation by Caspase-8[J].J Exp Med,2008,205(9):1967-1973.
    [45]
    Moriwaki K,Bertin J,Gough PJ,et al.A RIPK3-Caspase 8 complex mediates atypical pro-IL-1 beta processing[J].J Immunol,2015,194(4):1938-1944.
    [46]
    Vince JE,Wong WWL,Gentle I,et al.Inhibitor of apoptosis proteins limit RIP3 kinase-dependent interleukin-1 activation.[J].Immunity,2012,36(2):215-227.
    [47]
    Shenderov K,Riteau N,Yip R,et al.Cutting edge:endoplasmic reticulum stress licenses macrophages to produce mature IL-1β in response to TLR4 stimulation through a Caspase-8 and TRIF-dependent pathway[J].J Immunol,2014,192(5):2029-2033.
    [48]
    Bossaller L,Chiang PI,Schmidt-Lauber C,et al.Cutting edge:FAS(CD95)mediates noncanonical IL-1β and IL-18 maturation via Caspase-8 in an RIP3-independent manner[J].J Immunol,2012,189(12):5508-5512.
    [49]
    Uchiyama R,Yonehara S,Tsutsui H.Fas-mediated inflammatory response in Listeria monocytogene infection[J].J Immunol,2013,190(8):4245-4254.
    [50]
    Gringhuis SI,Kaptein TM,Wevers BA,et al.Dectin-1 is an extracellular pathogen sensor for the induction and processing of IL-1β via a noncanonical Caspase-8 inflammasome[J].Nat Immunol,2012,13(3):246-254.
    [51]
    Philip NH,Dillon CP,Snyder AG,et al.Caspase-8 mediates Caspase-1 processing and innate immune defense in response to bacterial blockade of NF-κB and MAPK signaling[J].Proc Natl Acad Sci U S A,2014,111(20):7385-7390.
    [52]
    Pasparakis M,Vandenabeele P.Necroptosis and its role in inflammation[J].Nature,2015,517(7534):311-320.
    [53]
    Andrew K,Jin CK,Tae BK,et al.Caspase-8 deficiency in epidermal keratinocytes triggers an inflammatory skin disease[J].J Exp Med,2009,206(10):2161-2177.
    [54]
    Saleh M,Mathison JC,Wolinski MK,et al.Enhanced bacterial clearance and sepsis resistance in Caspase-12-deficient mice[J].Nature,2006,440(7087):1064-1068.
    [55]
    Walle LV,Fernandez DJ,Demon D,et al.Does Caspase-12 suppress inflammasome activation[J].Nature,2016,534(7605):E1-U15.
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