N-methyl-d-aspartate receptor (NMDAR) encephalitis is the most common autoimmune encephalitis. It is usually treated by unselective depletion of B cells and plasma exchange to remove all antibodies. To create a more targeted treatment with fewer side effects, Reincke et al. engineered chimeric autoantibody receptor (CAAR) T cells, which express a multi-subunit NMDAR autoantigen linked to an intracellular signalling chain. Using serum from patients with NMDAR encephalitis, the construct was optimized for breadth of autoantibody binding. In a passive transfer mouse model, the CAAR T cells reduced NMDAR autoantibody levels in the serum and brain and eliminated autoreactive B cells, without signs of off-target toxicity or adverse events.