Pathogenic antibodies are active participants in spinal cord injury.
The role of B cells and autoimmunity as contributing factors to poor neurological outcomes following spinal cord injury (SCI) is poorly understood. The study by Ankeny et al., in this issue of the JCI, identifies a new immunopathological mechanism arising after SCI in mice (see the related article beginning on page 2990). The study shows that B cells produce pathogenic antibodies that impair lesion repair, resulting in worse neurological outcome. This new understanding of SCI disease pathogenesis, if confirmed in humans, reveals potential avenues for the development of novel neuroprotective immunotherapies.
Dekaban
Gregory A
GA
BioTherapeutics Research Laboratory, Molecular Brain Research Group, Robarts Research Institute and Department of Microbiology and Immunology,The University of Western Ontario, 100 Perth Drive, London, Ontario, Canada. dekaban@robarts.ca
Thawer
Sakina
S
D000818:Animals; D001323:Autoantibodies / Q000009:adverse effects / Q000276:immunology; D001402:B-Lymphocytes / Q000276:immunology*; D004195:Disease Models, Animal; D006801:Humans; D007167:Immunotherapy; D051379:Mice; D018345:Mice, Knockout; D009416:Nerve Regeneration / Q000502:physiology; D011379:Prognosis; D013119:Spinal Cord Injuries / Q000276:immunology* / Q000473:pathology* / Q000628:therapy
D001323:Autoantibodies