Lee Sang Hun, Sacks David L
Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, U.S.A.
Emerg Top Life Sci. 2017 Dec 22;1(6):621-626. doi: 10.1042/ETLS20170110.
Macrophages are considered a critical component of innate immunity against intracellular pathogens. Although macrophages have historically been viewed as monocyte-derived and terminally differentiated cells, recent progress has revealed that many tissue-resident macrophages are embryonically seeded, self-renewed, and perform homeostatic functions associated with M2-like activation programs. There is evidence that tissue-resident macrophages (TRMs) maintain their M2-like phenotype even in an infection-driven pro-inflammatory environment. In this regard, several intracellular pathogens are shown to exploit M2-like TRMs as replicative niches to evade pathogen-specific immunity. This knowledge provides a new perspective to understand the chronicity of infections and develop therapeutic strategies which can selectively target TRMs.
巨噬细胞被认为是针对细胞内病原体的固有免疫的关键组成部分。尽管巨噬细胞在历史上一直被视为单核细胞衍生的终末分化细胞，但最近的研究进展表明，许多组织驻留巨噬细胞是胚胎期植入、自我更新的，并执行与M2样激活程序相关的稳态功能。有证据表明，即使在感染驱动的促炎环境中，组织驻留巨噬细胞（TRMs）仍能维持其M2样表型。在这方面，几种细胞内病原体被证明利用M2样TRMs作为复制龛来逃避病原体特异性免疫。这一认识为理解感染的慢性化以及开发能够选择性靶向TRMs的治疗策略提供了新的视角。
