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破坏监测:抑制先天免疫的细菌III型分泌系统效应蛋白

Disabling surveillance: bacterial type III secretion system effectors that suppress innate immunity.

作者信息

Espinosa Avelina, Alfano James R

机构信息

Plant Science Initiative and The Department of Plant Pathology, University of Nebraska, Lincoln, NE 68588-0660, USA.

出版信息

Cell Microbiol. 2004 Nov;6(11):1027-40. doi: 10.1111/j.1462-5822.2004.00452.x.

Abstract

Many Gram-negative bacterial pathogens of plants and animals are dependent on a type III protein secretion system (TTSS). TTSSs translocate effector proteins into host cells and are capable of modifying signal transduction pathways. The innate immune system of eukaryotes detects the presence of pathogens using specific pathogen recognition receptors (PRRs). Plant PRRs include the FLS2 receptor kinase and resistance proteins. Animal PRRs include Toll-like receptors and nucleotide-binding oligomerization domain proteins. PRRs initiate signal transduction pathways that include mitogen-activated protein kinase (MAPK) cascades that activate defence-related transcription factors. This results in induction of proinflammatory cytokines in animals, and hallmarks of defence in plants including the hypersensitive response, callose deposition and the production of pathogenesis-related proteins. Several type III effectors from animal and plant pathogens have evolved to counteract innate immunity. For example, the Yersinia YopJ/P cysteine protease and the Pseudomonas syringae HopPtoD2 protein tyrosine phosphatase inhibits defence-related MAPK kinase activity in animals and plants respectively. Thus, type III effectors can suppress signal transduction pathways activated by PRR surveillance systems. Understanding targets and activities of type III effectors will reveal much about bacterial pathogenicity and the innate immune system in plants and animals.

摘要

许多动植物的革兰氏阴性细菌病原体都依赖于III型蛋白分泌系统(TTSS)。III型蛋白分泌系统将效应蛋白转运到宿主细胞中,并能够改变信号转导途径。真核生物的先天免疫系统使用特定的病原体识别受体(PRR)来检测病原体的存在。植物PRR包括FLS2受体激酶和抗性蛋白。动物PRR包括Toll样受体和核苷酸结合寡聚化结构域蛋白。PRR启动信号转导途径,其中包括激活与防御相关转录因子的丝裂原活化蛋白激酶(MAPK)级联反应。这导致动物体内促炎细胞因子的诱导,以及植物中防御的特征,包括超敏反应、胼胝质沉积和病程相关蛋白的产生。来自动植物病原体的几种III型效应器已经进化以对抗先天免疫。例如,耶尔森氏菌YopJ/P半胱氨酸蛋白酶和丁香假单胞菌HopPtoD2蛋白酪氨酸磷酸酶分别抑制动植物中与防御相关的MAPK激酶活性。因此,III型效应器可以抑制由PRR监测系统激活的信号转导途径。了解III型效应器的靶标和活性将揭示许多关于细菌致病性以及动植物先天免疫系统的信息。

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