Department of Microbiology, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Department of Microbiology, University of Texas Southwestern Medical Center, Dallas, Texas, USA
Infect Immun. 2018 Mar 22;86(4). doi: 10.1128/IAI.00560-17. Print 2018 Apr.
The enteric attaching and effacing (A/E) pathogens enterohemorrhagic (EHEC) and enteropathogenic (EPEC) and the invasive pathogens enteroinvasive (EIEC) and encode type III secretion systems (T3SS) used to inject effector proteins into human host cells during infection. Among these are a group of effectors required for NF-κB-mediated host immune evasion. Recent studies have identified several effector proteins from A/E pathogens and EIEC/ that are involved in suppression of NF-κB and have uncovered their cellular and molecular functions. A novel mechanism among these effectors from both groups of pathogens is to coordinate effector function during infection. This cooperativity among effector proteins explains how bacterial pathogens are able to effectively suppress innate immune defense mechanisms in response to diverse classes of immune receptor signaling complexes (RSCs) stimulated during infection.
肠侵袭和黏附(A/E)病原体肠出血性大肠杆菌(EHEC)和肠致病性大肠杆菌(EPEC)以及侵袭性病原体肠侵袭性大肠杆菌(EIEC)编码用于在感染期间将效应蛋白注入人体宿主细胞的 III 型分泌系统(T3SS)。其中有一组效应蛋白对于 NF-κB 介导的宿主免疫逃逸是必需的。最近的研究已经鉴定出来自 A/E 病原体和 EIEC/的几种效应蛋白,这些蛋白参与抑制 NF-κB,并揭示了它们的细胞和分子功能。这些来自两组病原体的效应蛋白的一个新机制是在感染过程中协调效应蛋白的功能。这种效应蛋白之间的协同作用解释了细菌病原体如何能够有效地抑制先天免疫防御机制,以响应感染期间刺激的不同类别的免疫受体信号复合物(RSCs)。