【摘要】：炎癥小體(Inflammasome)是細(xì)胞質(zhì)中多種蛋白組裝成的復(fù)合物,炎癥小體的激活能活化半胱天冬酶-1(caspase-1),進(jìn)而引起系列促炎細(xì)胞因子的成熟與分泌和誘導(dǎo)細(xì)胞焦亡。當(dāng)病原體感染時(shí),炎癥小體的激活在宿主天然免疫應(yīng)答中起重要作用。大量研究表明,多數(shù)情況下炎癥小體對宿主起保護(hù)作用,僅少數(shù)情況下保護(hù)作用不明顯或表現(xiàn)出有利于病原體生存的一面。在長期進(jìn)化中,病原體也發(fā)展出逃避宿主炎癥小體作用的策略。病原體可直接抑制炎癥小體的激活或減弱炎癥小體的作用。本文從病原體感染宿主中炎癥小體的作用及病原體對宿主炎性癥小體的逃避機(jī)制兩方面對二者相互作用的最新研究進(jìn)展進(jìn)行綜述。
[Abstract]:Inflammatory bodies (Inflammatory bodies) are a complex of proteins assembled in the cytoplasm. Activation of inflammatory bodies activates caspase-1, which induces the maturation and secretion of a series of pro-inflammatory cytokines and induces cell death. A large number of studies have shown that inflammatory corpuscles protect the host in most cases, but in only a few cases the protective effect is not obvious or appears to be beneficial to the survival of pathogens.Pathogens have also developed strategies to escape the role of host inflammatory corpuscles in long-term evolution.Pathogens can directly inhibit the activation of inflammatory corpuscles or weaken inflammation. This article reviews the latest research progress in the interaction between pathogens and inflammatory bodies in host infection and the escape mechanism of pathogens to host inflammatory bodies.
【作者單位】： 西南大學(xué)動(dòng)物科技學(xué)院;
【基金】：國家自然科學(xué)基金(31400762) 重慶市科委專項(xiàng)(cstc2015jcyjB X0108,cstc2015shmszx80022,cstc2015shmszx80010) 國家現(xiàn)代農(nóng)業(yè)(肉牛牦牛)產(chǎn)業(yè)技術(shù)體系建設(shè)專項(xiàng)基金(CARS-38) 中央高�；究蒲袠I(yè)務(wù)費(fèi)專項(xiàng)(XDJK2015B002,XDJK2016E036)~~
【分類號(hào)】：R392
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本文編號(hào)：2219707