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Neurology 2002;59:S7-S12
© 2002 American Academy of Neurology

Neurology supplements are not peer-reviewed. Information contained in Neurology supplements represent the opinions of the authors and are not endorsed by nor do they reflect the views of the American Academy of Neurology, Editor-in-Chief, or Associate Editors of Neurology.

Immune mechanisms in chronic inflammatory demyelinating neuropathy

Bernd C. Kieseier, MD, Marinos C. Dalakas, MD and Hans-Peter Hartung, MD

From the Department of Neurology (Drs. Kieseier and Hartung), Heinrich-Heine-Universität, Düsseldorf, Germany, and the Neuromuscular Diseases Section (Dr. Dalakas), National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD.

Address correspondence and reprint requests to Dr. Hans-Peter Hartung, Department of Neurology, Heinrich-Heine-Universität, Moorenstrasse 5, 40225 Düsseldorf, Germany.

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.




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