Department of Microbiology and Molecular Genetics, Michigan State University, East Lansing, MI, United States.
Department of Microbiology and Physiological Systems, University of Massachusetts Medical School, Worcester, MA, United States.
Front Immunol. 2018 Sep 12;9:2094. doi: 10.3389/fimmu.2018.02094. eCollection 2018.
Our understanding of the host response to infections has historically focused on "resistance" mechanisms that directly control pathogen replication. However, both pathogen effectors and antimicrobial immune pathways have the capacity to damage host tissue, and the ability to tolerate these insults can also be critical for host survival. These "tolerance" mechanisms may be equally as important as resistance to prevent disease in the context of a persistent infection, such as tuberculosis, when resistance mechanisms are ineffective and the pathogen persists in the tissue for long periods. Host tolerance encompasses a wide range of strategies, many of which involve regulation of the inflammatory response. Here we will examine general strategies used by macrophages and T cells to promote tolerance in the context of tuberculosis, and focus on pathways, such as regulation of inflammasome activation, that are emerging as common mediators of tolerance.
我们对宿主感染反应的理解历史上一直集中在直接控制病原体复制的“抗性”机制上。然而，病原体效应子和抗菌免疫途径都有能力损伤宿主组织，而耐受这些损伤的能力对于宿主的生存也可能至关重要。在持续感染的情况下，如结核病，当抗性机制无效且病原体在组织中长时间存在时，这些“耐受”机制可能与抗性一样重要，以防止疾病。宿主耐受涵盖了广泛的策略，其中许多涉及炎症反应的调节。在这里，我们将研究巨噬细胞和 T 细胞在结核病背景下促进耐受所使用的一般策略，并重点关注作为耐受共同介质的途径，如炎症小体激活的调节。
