Advances in chronic inflammatory demyelinating polyneuropathy: disease variants and inflammatory response mediators and modifiers.
Available data on the immunopathogenesis of chronic inflammatory demyelinating polyneuropathy remain still fragmentary and insufficient for a unified hypothesis. Macrophage-mediated demyelination appears to play a fundamental role and cytokines, especially tumour necrosis factor-alpha, participate in this process. The nature of antigen presenting cells, T-cell receptors, adhesion molecules between inflammatory cells and myelinated fibers and the apparent predominance of T helper cell 1-related cytokines need to be explored to design more specific immunotherapies. In chronic cases of chronic inflammatory demyelinating polyneuropathy, a concomitant axonal loss secondary to primary demyelination is common and should be taken into consideration in the design of future therapeutic strategies.
Dalakas
M C
MC
Neuromuscular Diseases Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892-1382, USA.
D000956:Antigens, Viral / Q000276:immunology*; D001706:Biopsy; D003131:Combined Modality Therapy; D016207:Cytokines / Q000276:immunology / Q000627:therapeutic use; D006801:Humans; D008264:Macrophages / Q000276:immunology; D009412:Nerve Fibers / Q000473:pathology; D020277:Polyradiculoneuropathy, Chronic Inflammatory Demyelinating / Q000175:diagnosis* / Q000276:immunology* / Q000628:therapy; D006377:T-Lymphocytes, Helper-Inducer / Q000276:immunology
D000956:Antigens, Viral; D016207:Cytokines