B Cell-Targeted Therapy with Anti-CD20 Monoclonal Antibody Reduced Secondary Tissue Damage and Enhanced Behavioural Recovery Following Experimental Spinal Cord Injury in Mice

Traumatic injury to the spinal cord activates B cells, which culminates in the synthesis of autoantibodies. The functional significance of this immune response is unclear. Antibodies produced after SCI caused pathology, in part by activating intraspinal complement and cells bearing Fc receptors. These data indicate that B cells, through the production of antibodies, affect pathology in SCI. There is increasing appreciation of the important role of B cells in spinal cord trauma and consequently, increasing interest in treating these disorders through B cell-depletion therapy. The purpose of this study was to investigate the effects of anti-CD20 mAb B cell depletion therapy within the first 24 hours of SCI. In this study, the T6-T7 vertebrae in three groups of mice were injured by a 50-g clip-induced compression method, and the anti-murine CD20 IgG2a antibody (clone 18B12, 1 mg/kg) was intravenously administered starting 1 hour and 6 hours postinjury. Animals were sacrified at 24 hours. The anti-CD20 antibody treatment caused significant attenuation of leukocyte infiltration, reactive oxygen species-associated enzymes, and secondary tissue damage. Basso-Beattie-Bresnahan (BBB) scores were significantly higher in anti-CD20-treated mice than controls 10 days postinjury.