Rheumatoid arthritis (RA) can be viewed as a disease of barrier failure, in which CX3CR1/TREM2 synovial tissue resident macrophages that form the lining barrier over cartilage and bone become fragmented and disorganized. However, how to therapeutically rebuild this barrier, and how macrophage states transition during repair, remain unclear. We engineered TR-Ab19, a mouse-selective agonistic antibody against TREM2, as a precision tool to initiate and interrogate barrier repair in vivo. TR-Ab19 engages TREM2 linked downstream signaling and redirects synovial macrophages from Clec4d inflammatory/proliferative programs toward TREM2CX3CR1Aqp1 barrier-like states, thereby rebuilding the lining barrier. Across collagen-induced arthritis (CIA) and serum-transfer arthritis (STA) models, TR-Ab19 reduces synovitis, preserves cartilage and bone microarchitecture, limits osteoclastogenesis, and attenuates systemic cytokines and B cell abnormalities. Single-cell RNA-seq with trajectory and cell cell communication analyses reveal a TREM2 dependent shift toward a barrier-dominant macrophage ecosystem. Together, these findings establish antibody-mediated reprogramming of resident synovial macrophages as a barrier-centered strategy for RA and provide a framework for instructing macrophage niches in chronic inflammation.