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English: Fig. 1. Possible pathogenic mechanisms of anti-NMDAR encephalitis (A) N-methyl-D-aspartate receptors (NMDARs) released by tumors and viral infected neurons are taken up by antigen presenting cells (APCs) after apoptosis occurs. APCs migrate to local lymph nodes, and with the cooperation of CD4+ T cells, naive B cells in lymph nodes become memory B cells and differentiate into plasma cells. These cells and anti-NMDAR antibodies produced by peripheral plasma cells enter the brain, and immune cells such as B cells further undergo stimulation and differentiation. (B) In patients, anti-NMDAR antibodies bind to the GluN1 subunits of synaptic and extrasynaptic NMDARs. This disrupts the interaction between NMDAR and ephrin type B2 (EphB2) receptor, resulting in decreased NMDAR and neuronal hypoactivity. But, antibodies can sometimes increase the opening of synaptic receptors before internalization which may explain the seizures.