Open Access
Article
Pathogenesis of chronic inflammatory demyelinating polyradiculoneuropathy
Kourosh Rezania1,Betul Gundogdu1,Betty Soliven1
1
Department of Neurology, The University of Chicago, 5841 S. Maryland Ave/MC2030, Chicago, IL, 60637, USA. bsoliven@neurology.bsd.uchicago.edu
DOI: 10.2741/1286 Volume 9 Issue 1, pp.939-945
Published: 01 January 2004
(This article belongs to the Special Issue Inflammatory disorders of the nervous system)
Abstract

Chronic inflammatory demyelinating polyneuropathy (CIDP) is a term applied to a spectrum of immune-mediated demyelinating neuropathies that are heterogeneous in clinical manifestations and probably in pathogenesis. Although histopathologic studies of CIDP have been complicated by a relapsing course of the inflammatory reaction and its predominance in proximal nerve segments, many clues point to involvement of both cellular and humoral immune factors in the pathogenesis. Uncertainties remain regarding the provoking antigen(s) and location of the initial T cell activation. Breakdown of blood nerve barrier by activated T cells and its cytokines is followed by a local intraneural immune response with recruitment of macrophages and secretion of toxic factors, which cause damage to the myelin and axons. Activated T cells may also induce B cells to produce antibodies against nerve/myelin antigens. This review summarizes our current knowledge of the immunopathogenesis and insight from animal models of CIDP.

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Kourosh Rezania, Betul Gundogdu, Betty Soliven. Pathogenesis of chronic inflammatory demyelinating polyradiculoneuropathy. Frontiers in Bioscience-Landmark. 2004. 9(1); 939-945.