Immune‐mediated demyelination

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Abstract
The Guillain‐Barré syndrome (GBS) and multiple sclerosis (MS) are though to result from aberranr immune responses to myelin antigens. Recent evidence to implicate the cytokine tunmor necrosis factor‐α(TNF‐α) and the intercellular adhesion molecule‐1(ICAM‐1) in the pathogenesis of these disorders is reviewed. In GBS, elevared serum concentrations of TNF‐α are detectable in 20 to 50% of patients. TNF‐α released from autoreactive T cells, macrophages, or microglia may contribute to inflammatory demyelinative processes by upregulating the expression of recognition molecules on antigen‐presenting cells; by cytotoxic damage to endothlium; by stimulating the secretion of inflammatory mediators; by directly injuring the myelin sheath; or by interfering with impluse propagation. Its pathogenic potential in GBS is underscored by findings in experimental autoimmune neuritis. Soluble ICAM‐1, originating from T cells, macrophages, endothelium, or glial cells, circulates at increases concentrations in serum and cerebrospinal fluid of patients with active MS. ICAM‐1 may be crucially involved in the migration of autoreactive T lymphocytes from blood to brain. Whether ICAM‐1 can serve as a maker of acute inflammatory events in ms associated with clinical relapses warrants further investigation. TNF‐α and ICAM‐1 coud be targets for antigen nonspecific treatment approaches to the inflammatory demyelinating diseases GBS and MS.