[Advances in the roles of synovial macrophage subsets in the pathogenesis of rheumatoid arthritis].

Abstract

The pathogenesis of rheumatoid arthritis (RA) is closely associated with subsets of synovial macrophages. Tissue-resident macrophages (TRMs) and monocyte-derived macrophages (MDMs) differ in origin, phenotypic polarization, and function. TRMs originate from embryonic precursors and help maintain synovial niche homeostasis by clearing apoptotic cells. In contrast, MDMs are recruited from circulating monocytes by chemokines, acquire pro-inflammatory phenotypes, and secrete TNF-α, IL-1β, and other factors that drive inflammation and bone destruction. These two populations dynamically coexist in the RA joint microenvironment: decreased TRM numbers lead to increased MDM infiltration, while pro-inflammatory signals from MDMs further impair TRM function, forming a vicious cycle. Targeting distinct macrophage subsets may offer novel therapeutic strategies for RA. This review summarizes the mechanisms and interaction networks of TRMs and MDMs in RA pathogenesis, with the aim of providing insights for precision immune intervention in RA.