慢性炎症性脱髓鞘性多发性神经病
自身抗体
医学
发病机制
多发性神经病
免疫学
髓鞘
多神经根神经病
多发性硬化
自身免疫性疾病
免疫球蛋白G
格林-巴利综合征
抗体
病理
内科学
中枢神经系统
作者
Wei Xing Yan,Jude Taylor,Susan Andrias‐Kauba,John D. Pollard
标识
DOI:10.1002/1531-8249(200006)47:6<765::aid-ana9>3.0.co;2-8
摘要
Chronic inflammatory demyelinating polyneuropathy (CIDP) is regarded as an autoimmune disorder, but no clearly defined autoimmune mechanism has been described. Although most patients respond to plasma exchange, no convincing role for autoantibodies has yet been demonstrated. In this study, we have successfully passively transferred disease using sera and purified IgG from 4 of 12 patients responsive to plasma exchange by bypassing the blood-nerve barrier by intraneural injection or opening it by activated T cells. The sera from CIDP patients or purified IgG produced marked conduction block and demyelination, but normal sera or IgG or that from patients with multiple sclerosis or other neuropathies did not. These observations strongly support an important role for anti-myelin/Schwann cell autoantibodies in the pathogenesis of CIDP at least in some patients.
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