Myelin oligodendrocyte glycoprotein-induced autoimmune encephalomyelitis is chronic/relapsing in perforin knockout mice, but monophasic in Fas- and Fas ligand-deficient lpr and gld mice

Détails

ID Serval
serval:BIB_93612463564F
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Myelin oligodendrocyte glycoprotein-induced autoimmune encephalomyelitis is chronic/relapsing in perforin knockout mice, but monophasic in Fas- and Fas ligand-deficient lpr and gld mice
Périodique
European Journal of Immunology
Auteur(s)
Malipiero  U., Frei  K., Spanaus  K. S., Agresti  C., Lassmann  H., Hahne  M., Tschopp  J., Eugster  H. P., Fontana  A.
ISSN
0014-2980 (Print)
Statut éditorial
Publié
Date de publication
12/1997
Volume
27
Numéro
12
Pages
3151-60
Notes
Journal Article
Research Support, Non-U.S. Gov't --- Old month value: Dec
Résumé
The expression and action of Fas/Fas ligand (FasL) in multiple sclerosis has been postulated as a major pathway leading to inflammatory demyelination. To formally test this hypothesis, C57BL/6-lpr and -gld mice, which due to gene mutation express Fas and FasL in an inactive form, were immunized with myelin oligodendrocyte glycoprotein peptide(35-55). Whereas in wild-type C57BL/6 mice, experimental autoimmune encephalomyelitis (EAE), was chronic/relapsing, EAE in lpr and gld mice was characterized by a lower incidence of disease and a monophasic course. This contrasts with C57BL/6 perforin knockout mice, which showed the most severe form of EAE of all mouse strains tested, the course being chronic relapsing. The difference noted cannot be attributed to an involvement of FasL in oligodendrocyte damage since oligodendrocytes are insensitive to FasL-mediated cytotoxicity in vitro, and since in the acute phase of EAE gld mice also show CD4+ T cell infiltrates with associated demyelination in brain and spinal cord. Unlike oligodendrocytes, astrocytes were killed by FasL in vitro. It remains to be established whether this latter finding explains the different disease course of lpr and gld mice compared to wild-type and perforin knockout mice.
Mots-clé
Animals Antigens, CD95/genetics/*immunology Chronic Disease Encephalomyelitis, Autoimmune, Experimental/genetics/*immunology/pathology Fas Ligand Protein Membrane Glycoproteins/genetics/*immunology Mice Mice, Knockout Myelin-Associated Glycoprotein/administration & dosage/*immunology Oligodendroglia/immunology/pathology Pore Forming Cytotoxic Proteins Recurrence
Pubmed
Web of science
Création de la notice
24/01/2008 16:19
Dernière modification de la notice
20/08/2019 15:56
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