期刊
JOURNAL OF NEUROCHEMISTRY
卷 99, 期 4, 页码 1073-1087出版社
WILEY
DOI: 10.1111/j.1471-4159.2006.04147.x
关键词
antibodies; autoimmunity; B cells; CNS injury; neuroinflammation
资金
- NIAID NIH HHS [T32 AI55411, AI37326] Funding Source: Medline
- NINDS NIH HHS [NS047175] Funding Source: Medline
Clinical and experimental data indicate that spinal cord injury (SCl) 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 SCl-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 SCl produces marked dysregulation of B cell function (i.e. autoimmunity) with pathological potential.
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