Srinivasan Lalitha, Ahlbrand Sarah, Briken Volker
Department of Cell Biology and Molecular Genetics, University of Maryland, College Park, Maryland 20742.
Cold Spring Harb Perspect Med. 2014 Jun 26;4(8):a022459. doi: 10.1101/cshperspect.a022459.
Mycobacterium tuberculosis (Mtb) has coevolved with humans for tens of thousands of years. It is thus highly adapted to its human host and has evolved multiple mechanisms to manipulate host immune responses to its advantage. One central host pathogen interaction modality is host cell death pathways. Host cell apoptosis is associated with a protective response to Mtb infection, whereas a necrotic response favors the pathogen. Consistently, Mtb inhibits host cell apoptosis signaling but promotes induction of programmed necrosis. The molecular mechanisms involved in Mtb-mediated host cell death manipulation, the consequences for host immunity, and the potential for therapeutic and preventive approaches will be discussed.
结核分枝杆菌（Mtb）已经与人类共同进化了数万年。因此，它高度适应其人类宿主，并进化出多种机制来操纵宿主免疫反应以使其自身受益。宿主细胞死亡途径是宿主与病原体相互作用的一种核心方式。宿主细胞凋亡与对Mtb感染的保护性反应相关，而坏死反应则有利于病原体。一致的是，Mtb抑制宿主细胞凋亡信号传导，但促进程序性坏死的诱导。本文将讨论Mtb介导的宿主细胞死亡操纵所涉及的分子机制、对宿主免疫的影响以及治疗和预防方法的潜力。
