Effector pathways in immune mediated central nervous system demyelination

Bernd C. Kieseier; Maria K. Storch; Juan J. Archelos; Gianvito Martino; Hans Peter Hartung

doi:10.1097/00019052-199906000-00011

Effector pathways in immune mediated central nervous system demyelination

Bernd C. Kieseier, Maria K. Storch, Juan J. Archelos, Gianvito Martino, Hans Peter Hartung

IRCCS Ospedale San Raffaele

Research output: Contribution to journal › Article › peer-review

Abstract

Multiple sclerosis is generally regarded to be a primarily T-cell driven disease. Recent evidence has refocused interest on antibodies. Adhesion molecules, matrix metalloproteinases, chemokines and cytokines, and nitric oxide and oxygen metabolites all participate in the amplification and effector stages of the disease.

Original language	English
Pages (from-to)	323-336
Number of pages	14
Journal	Current Opinion in Neurology
Volume	12
Issue number	3
DOIs	https://doi.org/10.1097/00019052-199906000-00011
Publication status	Published - 1999

ASJC Scopus subject areas

Neuroscience(all)

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10.1097/00019052-199906000-00011

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title = "Effector pathways in immune mediated central nervous system demyelination",

abstract = "Multiple sclerosis is generally regarded to be a primarily T-cell driven disease. Recent evidence has refocused interest on antibodies. Adhesion molecules, matrix metalloproteinases, chemokines and cytokines, and nitric oxide and oxygen metabolites all participate in the amplification and effector stages of the disease.",

author = "Kieseier, {Bernd C.} and Storch, {Maria K.} and Archelos, {Juan J.} and Gianvito Martino and Hartung, {Hans Peter}",

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AU - Hartung, Hans Peter

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AB - Multiple sclerosis is generally regarded to be a primarily T-cell driven disease. Recent evidence has refocused interest on antibodies. Adhesion molecules, matrix metalloproteinases, chemokines and cytokines, and nitric oxide and oxygen metabolites all participate in the amplification and effector stages of the disease.

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Effector pathways in immune mediated central nervous system demyelination

Abstract

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