Autor(es): Stoll G.

Resumo: Cytokines are immune mediators that orchestrate inflammatory responses. In autoimmune disorders of the nervous system such as the Guillain-Barré syndrome (GBS), and the corresponding animal model, experimental autoimmune neuritis (EAN), proinflammatory cytokines augment nerve infiltration by T-cells and contribute to macrophage-mediated demyelination. The local balance between pro- and antiinflammatory effects determines the clinical course. Cytokine expression in the nervous system is, however, not restricted to autoimmune disorders. Cytokines likewise contribute to infarct growth after focal cerebral ischemia, and under certain conditions convey neuroprotection. This short review summarizes selected aspects of cytokine actions during immune-mediated demyelination and cerebral ischemia. Elucidation of cytokine-mediated pathways of neurotoxicity and neuroprotection may not only improve stroke treatment, but, in addition may have a major impact on autoimmune diseases such as multiple sclerosis and GBS, in which axonal loss rather than demyelination determines long-term disability.

Imprenta: Revue Neurologique, v. 158, p. 887-891, 2002

Identificador do objeto digital: 10-2002-158-10C1-0035-3787-101019-ART3

Descritores: Guillain-Barre Syndrome - Cell ; Guillain-Barre Syndrome - Cytopathology ; Guillain-Barre Syndrome - Pathogenesis ; Guillain-Barre Syndrome - Proteins ; Guillain-Barre Syndrome - Autoimmunity ; Guillain-Barre Syndrome - Cytokines ; Guillain-Barre Syndrome - Inflammation ; Guillain-Barre Syndrome - Immunology

Data de publicação: 2002

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