Citation

Ankeny DP, Lucin KM, Sanders VM, McGaughy VM, Popovich PG. J. Neurochem. 2006; 99(4): 1073-1087.

Affiliation

Department of Molecular Virology, Immunology and Medical Genetics, The Ohio State University College of Medicine, Columbus, Ohio 43210, USA.

Copyright

(Copyright © 2006, John Wiley and Sons)

DOI

10.1111/j.1471-4159.2006.04147.x

PMID

17081140

Abstract

Clinical and experimental data indicate that spinal cord injury (SCI) elicits pathological T-cell responses. Implicit in these data, but poorly understood, is that B lymphocytes (B cells) also contribute to the delayed pathophysiology of spinal trauma. Here, for the first time, we show that experimental spinal contusion injury elicits chronic systemic and intraspinal B cell activation with the emergence of a B cell-dependent organ-specific and systemic autoimmune response. Specifically, using sera from spinal cord injured mice, immunoblots reveal oligoclonal IgG reactivity against multiple CNS proteins. We also show SCI-induced synthesis of autoantibodies that bind nuclear antigens including DNA and RNA. Elevated levels of anti-DNA antibodies are a distinguishing feature of systemic lupus erythematosus and, via their ability to cross-react with neuronal antigens, can cause neuropathology. We show a similar pathologic potential for the autoantibodies produced after SCI. Thus, mammalian SCI produces marked dysregulation of B cell function (i.e. autoimmunity) with pathological potential.

Language: en