Macrophages maintain a dynamic balance in physiology. Various known or unknown microenvironmental signals influence the polarization, activation and death of macrophages, which creates an imbalance that leads to disease. Rheumatoid arthritis (RA) is characterized by the massive infiltration of a variety of chronic inflammatory cells in synovia. Abundant activated macrophages found in RA synovia are an early hallmark of RA, and the number of these macrophages can be decreased after effective treatment. In RA, the proportion of M1 (pro‐inflammatory macrophages) is higher than that of M2 (anti‐inflammatory macrophages). The increased pro‐inflammatory ability of macrophages is related to their excessive activation and proliferation as well as an enhanced anti‐apoptosis ability. At present, there are no clinical therapies specific to macrophages in RA. Understanding the mechanisms and functional consequences of the heterogeneity of macrophages will aid in confirming their potential role in inflammation development. This review will outline RA‐related macrophage properties (focus on polarization, metabolism and apoptosis) as well as the origin of macrophages. The molecular mechanisms that drive macrophage properties also be elucidated to identify novel therapeutic targets for RA and other autoimmune disease.

中文翻译：

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靶向巨噬细胞在类风湿性关节炎中的新兴作用：关注极化、代谢和细胞凋亡

巨噬细胞在生理上保持动态平衡。各种已知或未知的微环境信号会影响巨噬细胞的极化、活化和死亡，从而造成导致疾病的失衡。类风湿性关节炎 (RA) 的特征是滑膜中多种慢性炎症细胞的大量浸润。在 RA 滑膜中发现大量活化的巨噬细胞是 RA 的早期标志，有效治疗后这些巨噬细胞的数量可以减少。在 RA 中，M1（促炎巨噬细胞）的比例高于 M2（抗炎巨噬细胞）。巨噬细胞促炎能力的增强与其过度活化和增殖以及增强的抗凋亡能力有关。目前，还没有针对 RA 中巨噬细胞的临床疗法。了解巨噬细胞异质性的机制和功能后果将有助于确认它们在炎症发展中的潜在作用。本综述将概述与 RA 相关的巨噬细胞特性（重点是极化、代谢和细胞凋亡）以及巨噬细胞的起源。还阐明了驱动巨噬细胞特性的分子机制，以确定 RA 和其他自身免疫性疾病的新治疗靶点。