Abstract

Macrophages are essential immune cells that play a critical role in immune defense, immune homeostasis, and immune surveillance within the body. In rheumatoid arthritis (RA), an autoimmune disease, increased infiltration of synovial macrophages leads to heightened secretion of pro-inflammatory cytokines such as IL-6 and TNF-α, resulting in joint erosion. Macrophages have the ability to switch their functions through a process called macrophage polarization, giving rise to two main phenotypes: inflammatory macrophages (M1) and anti-inflammatory macrophages (M2). In RA, the balance between M1 and M2 phenotypes influences the disease’s pathogenesis and prognosis. M1 macrophages secrete pro-inflammatory cytokines, contributing to joint erosion, while M2 macrophages support tissue repair. Consequently, targeting the local inflammatory response initiated by M1 macrophages is crucial in RA treatment. Biological agents that block inflammatory factors and chemokines induced by macrophages are being developed to combat RA. Additionally, extracellular vesicles can guide macrophage reprogramming, promoting the transition from M1 to anti-inflammatory M2 macrophages and restoring tissue homeostasis.

Full Text
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