CD 19 as a therapeutic target in a spontaneous autoimmune polyneuropathy

Summary Spontaneous autoimmune polyneuropathy ( SAP ) in B 7‐2 knock‐out non‐obese diabetic ( NOD ) mice is mediated by myelin protein zero ( P 0)‐reactive T helper type 1 ( T h1) cells. In this study, we investigated the role of B cells in SAP , focusing on CD 19 as a potential therapeutic target. We found that P 0‐specific plasmablasts and B cells were increased in spleens of SAP mice compared to wild‐type NOD mice. Depletion of B cells and plasmablasts with anti‐ CD 19 monoclonal antibody (m A b) led to attenuation of disease severity when administered at 5 months of age. This was accompanied by decreased serum immunoglobulin ( Ig)G and IgM levels, depletion of P 0‐specific plasmablasts and B cells, down‐regulation/internalization of surface CD 19 and increased frequency of CD 4 + regulatory T cells in spleens. We conclude that B cells are crucial to the pathogenesis of SAP , and that CD 19 is a promising B cell target for the development of disease‐modifying agents in autoimmune neuropathies.