Immune mechanisms in chronic inflammatory demyelinating neuropathy
Immune mechanisms in chronic inflammatory demyelinating neuropathy
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DOI：
10.1212/wnl.59.12_suppl_6.s7
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发表时间：
2002-12-24
期刊：
影响因子：
9.9
通讯作者：
Hartung, HP
中科院分区：
文献类型：
--
作者：
Kieseier, BC;Dalakas, MC;Hartung, HP
慢性炎症性脱髓鞘性多发性神经病（CIDP）是一种获得性、免疫介导的周围神经病。近年来，普通免疫学基本原理的应用拓宽了我们对这种神经病的病因和免疫发病机制的理解。尽管细胞和体液因素都受到影响，但数据仍然不完整，不足以形成统一的假设。本综述总结了与 CIDP 免疫发病机制相关的基本免疫机制的现有知识，并讨论了 T 细胞、活化的巨噬细胞、细胞因子、共刺激分子和抗髓磷脂抗体的作用。当前 CIDP 治疗方法中的一个重要因素是越来越多的人认识到继发于原发性脱髓鞘的伴随轴突损失。
Chronic inflammatory demyelinating polyneuropathy (CIDP) is an acquired, immune-mediated peripheral neuropathy. In recent years, the application of basic principles of general immunology has widened our understanding of the etiology and immunopathogenesis of this neuropathy. Although both cellular and humoral factors have been implicated, the data are still fragmentary and insufficient for a unified hypothesis. This review summarizes the present knowledge of the fundamental immune mechanisms related to the immunopathogenesis of CIDP and discusses the role of T cells, activated macrophages, cytokines, co-stimulatory molecules, and anti-myelin antibodies. An important factor in current approaches to the therapy of CIDP is the increasingly recognized concomitant axonal loss that occurs secondary to primary demyelination.