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炎症小体蛋白AIM2负调节抗RNA病毒反应发生
作者:李健  刘雪  杨硕 
单位:南京医科大学 基础医学院, 江苏 南京 211166
关键词:炎症小体 AIM2 巨噬细胞 抗病毒反应 
分类号:R392.1
出版年·卷·期(页码):2018·37·第二期(220-225)
摘要:

目的:探索炎症小体蛋白AIM2在抗RNA病毒反应中的作用。方法:在野生型和AIM2基因敲除的巨噬细胞上感染不同RNA病毒,感染一定时间后用流式细胞仪检测病毒含量,用定量PCR和ELISA检测抗病毒基因和炎症因子表达,并用Western blot检测抗病毒信号通路蛋白的激活。结果:相对于野生型巨噬细胞,AIM2基因敲除细胞在RNA病毒感染后有更少的病毒存在,并且抗病毒效应分子在AIM2敲除细胞中表达明显升高,此外AIM2基因敲除可促进RNA抗病毒通路TBK1、IRF3和IKBα的激活。结论:炎症小体蛋白AIM2负调节抗RNA病毒反应。

Objective:To investigate the roles of AIM2 in anti-RNA viral response. Methods:WT and Aim2-/- BMDMs were infected with various RNA virus and after infection infected cells (GFP+) were counted by FACS and the expressions of antiviral cytokines at gene and protein levels were detected by real-time PCR (q-PCR) and ELISA. Finally the activation of antiviral pathway was detected by using Western blot. Results:Compared to WT BMDM, Aim2-/- cell had less RNA viral infection and higher antiviral cytokines production triggered by RNA virus. Consistently, the activation of TBK1, IRF3 and IKBα represented by phosphorylation was upregulated in Aim2 deficient cells in response to RNA viral infection. Conclusion:The results clearly demonstrate the negative role of AIM2 in anti-RNA viral response.

参考文献:

[1] SCHRODER K,TSCHOPP J.The inflammasomes[J].Cell,2010,140(6):821-832.
[2] LIU X,ZHANG Z,RUAN J,et al.Inflammasome-activated gasdermin D causes pyroptosis by forming membrane pores[J].Nature,2016,535(7610):153-158.
[3] SHI J,ZHAN Y,WANG K,et al.Cleavage of GSDMD by inflammatory caspases determines pyroptotic cell death[J].Nature,2015,526(7575):660-665.
[4] RATHINAM V A,VANAJA S K,FITZGERALD K A.Regulation of inflammasome signaling[J].Nat Immunol,2012,13(4):333-342.
[5] WANG X,JIANG W,YAN Y,et al.RNA viruses promote activation of the NLRP3 inflammasome through a RIP1-RIP3-DRP1 signaling pathway[J].Nat Immunol,2014,15(12):1126-1133.
[6] WANG Y,NING X,GAO P,et al.Inflammasome activation triggers caspase-1-mediated cleavage of cGAS to regulate responses to DNA virus infection[J].Immunity,2017,46(3):393-404.
[7] JOUNG S M,PARK Z Y,RANI S,et al.Akt contributes to activation of the TRIF-dependent signaling pathways of TLRs by interacting with TANK-binding kinase 1[J].J Immunol,2011,186(1):499-507.
[8] WILSON J E,PETRUCELLI A S,CHEN L,et al.Inflammasome-independent role of AIM2 in suppressing colon tumorigenesis via DNA-PK and Akt[J].Nat Med,2015,21(8):906-913.
[9] IVASHKIV L B,DONLIN L T.Regulation of type Ⅰ interferon responses[J].Nat Rev Immunol,2014,14(1):36-49.
[10] 苏卫东,陈磊.RIG-Ⅰ样受体在抗RNA病毒免疫和治疗中的进展[J].现代医学,2015,43(11):1456-1459.

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