巨噬细胞程序性坏死在肝脏免疫应答中的作用

周思敏; 郭丽萍; 张君; 周璐; 王邦茂

doi:10.3969/j.issn.1001-5256.2020.02.048

巨噬细胞程序性坏死在肝脏免疫应答中的作用

DOI: 10.3969/j.issn.1001-5256.2020.02.048

天津医科大学总医院消化科

基金项目:

国家自然科学基金地区基金项目(81860109)；

详细信息

中图分类号: R575
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- 被引次数: 0
出版历程
- 收稿日期: 2019-07-29
- 出版日期: 2020-02-20

Programmed necrosis of macrophages plays an important role in liver immune response

Department of Gastroenterology,Tianjin Medical University General Hospital

Research funding:

摘要

摘要:
肝脏巨噬细胞持续接受抗原的刺激,处于免疫耐受及免疫应答的动态平衡状态。肝脏巨噬细胞对肝外抗原的免疫应答与肝脏的免疫稳态密切相关,程序性坏死通路是调控其功能和存亡的关键通路。回顾了程序性坏死通路与凋亡通路的关系,具体阐述了IKK复合物的活性在程序性坏死和凋亡通路交互调控中的重要作用。程序性坏死在肝脏巨噬细胞对肝外抗原的应答中的作用仍然有待阐明。
- 肝疾病 /
- 巨噬细胞 /
- 凋亡 /
- 程序性坏死 /
- 免疫系统现象
Abstract:
Liver macrophages are in a dynamic equilibrium of immune tolerance and immune response after continuous antigen stimulation.The immune response of liver macrophages to external antigen is closely associated with the immune homeostasis of the liver. This article reviews the association between the programmed necrosis pathway and the apoptotic pathway and elaborates on the important role of the activity of IKK complex in the interactive regulation of the programmed necrosis and apoptotic pathways. Further studies are needed to clarify the role of programmed necrosis in the response of liver macrophages to extrahepatic antigens.
- liver diseases /
- macrophages /
- apoptosis /
- programmed necrosis /
- immune system phenomena

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参考文献(50)

[1] BERTRAND MJ,MILUTINOVIC S,DICKSON KM,et al. cIAP1and cIAP2 facilitate cancer cell survival by functioning as E3ligases that promote RIP1 ubiquitination[J]. Mol Cell,2008,30(6):689-700.

[2] ZHANG DW,SHAO J,LIN J,et al. RIP3,an energy metabolism regulator that switches TNF-induced cell death from apoptosis to necrosis[J]. Science,2009,325(5938):332-336.

[3] ZHANG YF,HE W,ZHANG C,et al. Role of receptor interacting protein(RIP)1 on apoptosis-inducing factor-mediated necroptosis during acetaminophen-evoked acute liver failure in mice[J]. Toxicol Lett,2014,225(3):445-453.

[4] ZHOU L,BRAAT H,FABER KN,et al. Monocytes and their pathophysiological role in Crohn’s disease[J]. Cell Mol Life Sci,2009,66(2):192-202.

[5] LIU BS,JANSSEN HL,BOONSTRA A. Type I and III interferons enhance IL-10R expression on human monocytes and macrophages,resulting in IL-10-mediated suppression of TLR-induced IL-12[J]. Eur J Immunol,2012,42(9):2431-2440.

[6] BÉLAND K,LAPIERRE P,DJILALI-SAIAH I,et al. Liver restores immune homeostasis after local inflammation despite the presence of autoreactive T cells[J]. PLo S One,2012,7(10):e48192.

[7] LONGHI MS,MITRY RR,SAMYN M,et al. Vigorous activation of monocytes in juvenile autoimmune liver disease escapes the control of regulatory T-cells[J]. Hepatology,2009,50(1):130-142.

[8] CARPENTER HA,CZAJA AJ. The role of histologic evaluation in the diagnosis and management of autoimmune hepatitis and its variants[J]. Clin Liver Dis,2002,6(3):685-705.

[9] SUNAMI Y,LEITÄUSER F,GUL S,et al. Hepatic activation of IKK/NFκB signaling induces liver fibrosis via macrophagemediated chronic inflammation[J]. Hepatology,2012,56(3):1117-1128.

[10] ZHANG J,GUO L,LIU M,et al. Receptor-interacting protein kinase 3 mediates macrophage/monocyte activation in autoimmune hepatitis and regulates interleukin-6 production[J]. United European Gastroenterol J,2018,6(5):719-728.

[11] MARTYNOVA TV,ALEKSIEIEVA IM. Functional activity of peritonal macrophages in liver immune damage of cellular and antibody genesis in mice[J]. Fiziol Zh,2009,55(1):36-42.

[12] DEUTSCH M,GRAFFEO CS,ROKOSH R,et al. Divergent effects of RIP1 or RIP3 blockade in murine models of acute liver injury[J]. Cell Death Dis,2015,6:e1759.

[13] HUMPHRIES F,YANG S,WANG B,et al. RIP kinases:Key decision makers in cell death and innate immunity[J]. Cell Death Differ,2015,22(2):225-236.

[14] RICKARD JA,O’DONNELL JA,EVANS JM,et al. RIPK1 regulates RIPK3-MLKL-driven systemic inflammation and emergency hematopoiesis[J]. Cell,2014,157(5):1175-1188.

[15] KIM SJ,LEE SM. Necrostatin-1 protects against D-galactosamine and lipopolysaccharide-induced hepatic injury by preventing TLR4 and RAGE signaling[J]. Inflammation,2017,40(6):1912-1923.

[16] STOPPE C,AVERDUNK L,GOETZENICH A,et al. The protective role of macrophage migration inhibitory factor in acute kidney injury after cardiac surgery[J]. Sci Transl Med,2018,10(441):eaan4886.

[17] YANG J,ZHAO Y,ZHANG L,et al. RIPK3/MLKL-mediated neuronal necroptosis modulates the M1/M2 polarization of microglia/macrophages in the ischemic cortex[J]. Cereb Cortex,2018,28(7):2622-2635.

[18] WILKINS KA,BANCROFT J,BOSCH M,et al. Reactive oxygen species and nitric oxide mediate actin reorganization and programmed cell death in the self-incompatibility response of papaver[J]. Plant Physiol,2011,156(1):404-416.

[19] CAI Z,JITKAEW S,ZHAO J,et al. Plasma membrane translocation of trimerized MLKL protein is required for TNF-induced necroptosis[J]. Nat Cell Biol,2014,16(1):55-65.

[20] WANG H,SUN L,SU L,et al. Mixed lineage kinase domainlike protein MLKL causes necrotic membrane disruption upon phosphorylation by RIP3[J]. Mol Cell,2014,54(1):133-146.

[21] CHEN X,LI W,REN J,et al. Translocation of mixed lineage kinase domain-like protein to plasma membrane leads to necrotic cell death[J]. Cell Res,2014,24(1):105-121.

[22] KACZMAREK A,VANDENABEELE P,KRYSKO DV. Necroptosis:The release of damage-associated molecular patterns and its physiological relevance[J]. Immunity,2013,38(2):209-223.

[23] WEINLICH R,OBERST A,DILLON CP,et al. Protective roles for caspase-8 and cFLIP in adult homeostasis[J]. Cell Rep,2013,5(2):340-348.

[24] KRYSKO DV,GARG AD,KACZMAREK A,et al. Immunogenic cell death and DAMPs in cancer therapy[J]. Nat Rev Cancer,2012,12(12):860-875.

[25] NI HM,CHEN X,DING WX,et al. Differential roles of JNK in Con A/Gal N and Con A-induced liver injury in mice[J]. Am J Pathol,2008,173(4):962-972.

[26] MORIWAKI K,CHAN FK. RIP3:A molecular switch for necrosis and inflammation[J]. Genes Dev,2013,27(15):1640-1649.

[27] MICHEAU O,TSCHOPP J. Induction of TNF receptor I-mediated apoptosis via two sequential signaling complexes[J].Cell,2003,114(2):181-190.

[28] HÄCKER H,KARIN M. Regulation and function of IKK and IKK-related kinases[J]. Sci STKE,2006,2006(357):re13.

[29] BRUMMELKAMP TR,NIJMAN SM,DIRAC AM,et al. Loss of the cylindromatosis tumour suppressor inhibits apoptosis by activating NF-kappaB[J]. Nature,2003,424(6950):797-801.

[30] KOVALENKO A,CHABLE-BESSIA C,CANTARELLA G,et al.The tumour suppressor CYLD negatively regulates NF-kappaB signalling by deubiquitination[J]. Nature,2003,424(6950):801-805.

[31] SCHWORER SA,SMIRNOVA II,KURBATOVA I,et al. Tolllike receptor-mediated down-regulation of the deubiquitinase cylindromatosis(CYLD)protects macrophages from necroptosis in wild-derived mice[J]. J Biol Chem,2014,289(20):14422-14433.

[32] LEGARDA D,JUSTUS SJ,ANG RL,et al. CYLD proteolysis protects macrophages from TNF-mediated auto-necroptosis induced by LPS and licensed by type I IFN[J]. Cell Rep,2016,15(11):2449-2461.

[33] FENG S,YANG Y,MEI Y,et al. Cleavage of RIP3 inactivates its caspase-independent apoptosis pathway by removal of kinase domain[J]. Cell Signal,2007,19(10):2056-2067.

[34] CHO YS,CHALLA S,MOQUIN D,et al. Phosphorylationdriven assembly of the RIP1-RIP3 complex regulates programmed necrosis and virus-induced inflammation[J]. Cell,2009,137(6):1112-1123.

[35] MOQUIN DM,MCQUADE T,CHAN FK. CYLD deubiquitinates RIP1 in the TNFα-induced necrosome to facilitate kinase activation and programmed necrosis[J]. PLo S One,2013,8(10):e76841.

[36] MORIOKA S,BROGLIE P,OMORI E,et al. TAK1 kinase switches cell fate from apoptosis to necrosis following TNF stimulation[J]. J Cell Biol,2014,204(4):607-623.

[37] DONDELINGER Y,JOUAN-LANHOUET S,DIVERT T,et al.NF-κB-independent role of IKKα/IKKβin preventing RIPK1kinase-dependent apoptotic and necroptotic cell death during TNF signaling[J]. Mol Cell,2015,60(1):63-76.

[38] DONDELINGER Y,DARDING M,BERTRAND MJ,et al. Poly-ubiquitination in TNFR1-mediated necroptosis[J]. Cell Mol Life Sci,2016,73(11-12):2165-2176.

[39] WILSON NS,DIXIT V,ASHKENAZI A. Death receptor signal transducers:Nodes of coordination in immune signaling networks[J]. Nat Immunol,2009,10(4):348-355.

[40] NEWTON K,DUGGER DL,WICKLIFFE KE,et al. Activity of protein kinase RIPK3 determines whether cells die by necroptosis or apoptosis[J]. Science,2014,343(6177):1357-1360.

[41] MANDAL P,BERGER SB,PILLAY S,et al. RIP3 induces apoptosis independent of pronecrotic kinase activity[J]. Mol Cell,2014,56(4):481-495.

[42] KURIAKOSE T,MAN SM,MALIREDDI RK,et al. ZBP1/DAI is an innate sensor of influenza virus triggering the NLRP3 inflammasome and programmed cell death pathways[J]. Sci Immunol,2016,1(2):aag2045.

[43] CHIU CC,HUANG YT,WANG YC,et al. Pretreatment with lipopolysaccharide ameliorates Pseudomonas exotoxin A-induced hepatotoxicity in rats[J]. Immunopharmacol Immunotoxicol,2013,35(2):296-303.

[44] TRIVEDI PJ,ADAMS DH. Gut-liver immunity[J]. J Hepatol,2016,64(5):1187-1189.

[45] WEI Y,ZENG B,CHEN J,et al. Enterogenous bacterial glycolipids are required for the generation of natural killer T cells mediated liver injury[J]. Sci Rep,2016,6:36365.

[46] MANFREDO VS,HILTENSPERGER M,KUMAR V,et al. Translocation of a gut pathobiont drives autoimmunity in mice and humans[J]. Science,2018,359(6380):1156-1161.

[47] BLÉRIOT C,DUPUIS T,JOUVION G,et al. Liver-resident macrophage necroptosis orchestrates type 1 microbicidal inflammation and type-2-mediated tissue repair during bacterial infection[J]. Immunity,2015,42(1):145-158.

[48] PAMER EG. Immune responses to Listeria monocytogenes[J]. Nat Rev Immunol,2004,4(10):812-823.

[49] HE S,LIANG Y,SHAO F,et al. Toll-like receptors activate programmed necrosis in macrophages through a receptor-interacting kinase-3-mediated pathway[J]. Proc Natl Acad Sci U S A,2011,108(50):20054-20059.

[50] MA Y,TEMKIN V,LIU H,et al. NF-kappaB protects macrophages from lipopolysaccharide-induced cell death:The role of caspase 8 and receptor-interacting protein[J]. J Biol Chem,2005,280(51):41827-41834.

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