Hamidzadeh Kajal, Christensen Stephen M, Dalby Elizabeth, Chandrasekaran Prabha, Mosser David M
Department of Cell Biology and Molecular Genetics, Maryland Pathogen Research Institute, University of Maryland, College Park, Maryland 20742; email:
Annu Rev Physiol. 2017 Feb 10;79:567-592. doi: 10.1146/annurev-physiol-022516-034348. Epub 2016 Dec 7.
In recent years, researchers have devoted much attention to the diverse roles of macrophages and their contributions to tissue development, wound healing, and angiogenesis. What should not be lost in the discussions regarding the diverse biology of these cells is that when perturbed, macrophages are the primary contributors to potentially pathological inflammatory processes. Macrophages stand poised to rapidly produce large amounts of inflammatory cytokines in response to danger signals. The production of these cytokines can initiate a cascade of inflammatory mediator release that can lead to wholesale tissue destruction. The destructive inflammatory capability of macrophages is amplified by exposure to exogenous interferon-γ, which prolongs and heightens inflammatory responses. In simple terms, macrophages can thus be viewed as incendiary devices with hair triggers waiting to detonate. We have begun to ask questions about how these cells can be regulated to mitigate the collateral destruction associated with macrophage activation.
近年来，研究人员十分关注巨噬细胞的多种作用及其在组织发育、伤口愈合和血管生成中的贡献。在关于这些细胞多样生物学特性的讨论中不应被忽视的是，一旦受到干扰，巨噬细胞就是潜在病理性炎症过程的主要促成因素。巨噬细胞随时准备响应危险信号，迅速产生大量炎性细胞因子。这些细胞因子的产生可引发一系列炎性介质的释放，进而导致大规模组织破坏。暴露于外源性干扰素-γ会放大巨噬细胞的破坏性炎症能力，从而延长并增强炎症反应。简而言之，巨噬细胞可被视为一触即发、随时准备引爆的燃烧装置。我们已开始探究如何调节这些细胞，以减轻与巨噬细胞激活相关的附带损害。
