Perforin and tumor necrosis factor alpha in the pathogenesis of experimental allergic encephalomyelitis: comparison of autoantigen induced and transferred disease in Lewis rats.

Détails

ID Serval
serval:BIB_5110F0E48458
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Perforin and tumor necrosis factor alpha in the pathogenesis of experimental allergic encephalomyelitis: comparison of autoantigen induced and transferred disease in Lewis rats.
Périodique
Journal of autoimmunity
Auteur(s)
Held W., Meyermann R., Qin Y., Mueller C.
ISSN
0896-8411
Statut éditorial
Publié
Date de publication
1993
Peer-reviewed
Oui
Volume
6
Numéro
3
Pages
311-322
Langue
anglais
Notes
Publication types: Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
Publication Status: ppublish
Résumé
A cell-mediated cytotoxic reaction is believed to be involved in inflammatory lesion formation of experimental allergic encephalomyelitis (EAE). We compared EAE diseased animals which had either been immunized with myelin basic protein (MBP) or adoptively received MBP specific T-cell lines in order to study whether the different courses of disease induction are reflected by quantitative or qualitative differences in the expression of genes encoding putative mediators of tissue damage, i.e. TNF alpha, and the pore-forming protein perforin. With the appearance of signs of paralysis, both genes are induced in cells within the CNS lesions, whereas drastically reduced numbers of TNF alpha- and perforin gene-expressing cells are observed during recovery, despite the presence of high numbers of mononuclear cells in the CNS. Marked differences, however, exist in the gene expression profiles: during the phase of most severe clinical signs TNF alpha expressing cells are 2 to 3 times more frequent in transferred than immunized animals. In animals with MBP-induced EAE the number of perforin expressing cells represents only 1.6% of the IL2R gene expressing cells, while this fraction represents 25% in mice which received autoaggressive T cells. Thus, the presence of a high number of activated killer cells may accelerate tissue damage and progression of disease in passive EAE whereas in actively induced EAE activation of regulatory mechanisms induced by polyclonal activation after immunization may prevent generation of large amounts of activated cytotoxic T cells.
Mots-clé
Animals, Autoantigens/immunology, Encephalomyelitis, Autoimmune, Experimental/immunology, Encephalomyelitis, Autoimmune, Experimental/pathology, Gene Expression Regulation/immunology, Guinea Pigs, Immunotherapy, Adoptive, Membrane Glycoproteins/biosynthesis, Membrane Glycoproteins/genetics, Myelin Basic Proteins/immunology, Perforin, Pore Forming Cytotoxic Proteins, RNA, Messenger/metabolism, Rats, Rats, Inbred Lew, Receptors, Interleukin-2/genetics, T-Lymphocytes/immunology, Tumor Necrosis Factor-alpha/biosynthesis, Tumor Necrosis Factor-alpha/genetics
Pubmed
Web of science
Création de la notice
17/01/2008 16:24
Dernière modification de la notice
03/03/2018 17:10
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