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Immunological markers in multiple sclerosis

Articolo
Data di Pubblicazione:
2000
Citazione:
Immunological markers in multiple sclerosis / Gironi, M., Bergami, A., Brambilla, E., Ruffini, F., Furlan, R., Comi, G., Martino, G.. - In: NEUROLOGICAL SCIENCES. - ISSN 1590-1874. - 21:8(2000), pp. 871-875.
Abstract:
Multiple sclerosis (MS) is characterized by the presence in the central nervous system (CNS) of perivascular inflammatory infiltrates containing, among others, autoreactive T cells and activated macrophages. These observations indicate that MS is a T cell-mediated CNS-confined chronic inflammatory demyelinating disease in which the ultimate effector cell is the activated macrophage. The inflammatory process, leading to patchy demyelination and axonal loss, is mainly sustained by pro-inflammatory cytokines that, along with chemokines, adhesion molecules and metalloproteases, modulate at different levels the pathogenic process underlying MS. Due to their central role in MS pathogenesis, "inflammatory" molecules might represent suitable peripheral markers of disease (disease-trait) and/or disease activity (state-trait). However, reliable disease-trait or state-trait immunological markers for MS have not yet been identified. The intrinsic characteristics of these molecules (i.e. autocrine/paracrine activity, short half-life, redundancy) may in part explain their inconsistency as disease markers. Additionally, the unreliability of methodologies and the lack of careful patient stratification can also, at least in part, account for the unsatisfactory results so far obtained. © Springer-Verlag 2000.
Tipologia CRIS:
1.1 Articolo in rivista
Keywords:
Adhesion molecules; Chemokines; Cytokines; Disease-trait markers; Metalloproteases; State-trait markers
Elenco autori:
Gironi, M.; Bergami, A.; Brambilla, E.; Ruffini, F.; Furlan, R.; Comi, G.; Martino, G.
Autori di Ateneo:
FURLAN ROBERTO
MARTINO GIANVITO
Link alla scheda completa:
https://iris.unisr.it/handle/20.500.11768/205357
Pubblicato in:
NEUROLOGICAL SCIENCES
Journal
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