[The pathogenic role of inflammation in multiple sclerosis].
BACKGROUND
Multiple sclerosis (MS) is characterized by the presence in the central nervous system (CNS) of perivascular inflammatory infiltrates containing auto-reactive T and B cells and activated macrophages thus indicating that MS is a T cell-mediated CNS-confined chronic inflammatory demyelinating disease in which the ultimate effector cell is the activated macrophage.


METHODS
The inflammatory process, leading to patchy demyelination and axonal loss, is mainly sustained by pro-inflammatory cytokines that modulate at different levels the pathogenic process underlying MS. Cytokines can 1. Sustain the 'putative' CNS-confined inflammatory process leading to the development of myelin-specific T cells; 2. Activate circulating myelin-specific T cells and shape their repertoire (Th1 versus Th2 pattern); 3. Induce the CNS recruitment of non antigen specific T cells and myelinotoxic effector cells (monocyte/macrophages) from the periphery, and 4. Cause direct oligodendrotoxicity (TNF alpha) or induce the secretion of myelinotoxic substances. The present chapter will focus on the mechanisms sustaining the activity of pro-inflammatory cytokines in MS pathogenesis.
Departamento de Neurología, Istituto Scientifico San Raffaele, Milán, Italia. g.martino@hsr.it
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G
Martino
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R
Furlan
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PL
Poliani
D001921:Brain / Q000378:metabolism / Q000473:pathology*; D016207:Cytokines / Q000378:metabolism; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism; D009103:Multiple Sclerosis / Q000378:metabolism / Q000473:pathology*; D009457:Neuroglia / Q000378:metabolism; D013601:T-Lymphocytes / Q000378:metabolism
D016207:Cytokines; D018836:Inflammation Mediators