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Titolo:
Chemokine expression in GKO mice (lacking interferon-gamma) with experimental autoimmune encephalomyelitis
Autore:
Glabinski, AR; Krakowski, M; Han, YL; Owens, T; Ransohoff, RM;
Indirizzi:
Cleveland Clin Fdn, Lerner Res Inst, Dept Neurosci, Cleveland, OH 44195 USA Cleveland Clin Fdn Cleveland OH USA 44195 urosci, Cleveland, OH 44195 USA Med Univ Lodz, Dept Neurol, PL-90153 Lodz, Poland Med Univ Lodz Lodz Poland PL-90153 z, Dept Neurol, PL-90153 Lodz, Poland Montreal Neurol Inst, Montreal, PQ, Canada Montreal Neurol Inst Montreal PQ Canada eurol Inst, Montreal, PQ, Canada McGill Univ, Montreal, PQ, Canada McGill Univ Montreal PQ CanadaMcGill Univ, Montreal, PQ, Canada
Titolo Testata:
JOURNAL OF NEUROVIROLOGY
fascicolo: 1, volume: 5, anno: 1999,
pagine: 95 - 101
SICI:
1355-0284(199902)5:1<95:CEIGM(>2.0.ZU;2-1
Fonte:
ISI
Lingua:
ENG
Soggetto:
EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS; CENTRAL-NERVOUS-SYSTEM; MONOCYTE CHEMOATTRACTANT PROTEIN-1; TUMOR-NECROSIS-FACTOR; MULTIPLE-SCLEROSIS BRAIN; MESSENGER-RNA; IFN-GAMMA; GENE-EXPRESSION; CYTOKINES; DISEASE;
Keywords:
chemotactic factors; demyelinating diseases; type II interferon; mice; knockout;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
37
Recensione:
Indirizzi per estratti:
Indirizzo: Ransohoff, RM ClevelandCleveland, Lerner Res Inst, Dept Neurosci, 9500 Euclid Ave,NC 30, Cleveland Clin Fdn 9500 Euclid Ave,NC 30 Cleveland OH USA 44195
Citazione:
A.R. Glabinski et al., "Chemokine expression in GKO mice (lacking interferon-gamma) with experimental autoimmune encephalomyelitis", J NEUROVIRO, 5(1), 1999, pp. 95-101

Abstract

Experimental autoimmune encephalomyelitis (EAE) is an inflammatory diseaseof the central nervous system (CNS) considered to be an animal model for multiple sclerosis (MS). The detailed mechanism that specifies accumulation of inflammatory cells within the CNS in these conditions remains a subject of active investigation. Chemokines including IP-10, GRO-alpha, MCP-1 are produced in EAE tissues selectively by parenchymal astrocytes, but the regulatory stimuli that govern this expression remain undetermined. The unexpected occurrence of increased EAE susceptibility in Balb/c GKO mice (lacking IFN-gamma) offered an opportunity to examine the spectrum of chemokine expression during immune-mediated inflammation in the absence of a single regulatory cytokine. We found that chemokines MCP-1 and GRO-alpha were upregulated in the CNS of mice with EAE despite the GKO genotype. IP-10, which is highly expressed in the CNS of mice with an intact IFN-gamma gene and EAE, wasstrikingly absent, in vitro experiments confirmed that IFN gamma selectively stimulates astrocytes for IP-10 expression. These results indicate that IP-10 is dependent upon IFN-gamma for its upregulation during this model disease, and document directly that astrocyte expression of chemokines duringEAE is governed by pro-inflammatory cytokines.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 21/01/21 alle ore 02:51:07