Production of prostaglandin E2 and collagenase is inhibited by the recombinant soluble tumour necrosis factor receptor p55-human gamma 3 fusion protein at concentrations a hundred-fold lower than those decreasing T cell activation.

Détails

ID Serval
serval:BIB_857A1A89D725
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Production of prostaglandin E2 and collagenase is inhibited by the recombinant soluble tumour necrosis factor receptor p55-human gamma 3 fusion protein at concentrations a hundred-fold lower than those decreasing T cell activation.
Périodique
European Cytokine Network
Auteur(s)
Nicod L.P., Isler P., Chicheportiche R., Songeon F., Dayer J.M.
ISSN
1148-5493[print], 1148-5493[linking]
Statut éditorial
Publié
Date de publication
1996
Volume
7
Numéro
4
Pages
757-763
Langue
anglais
Résumé
TNF-alpha and lymphotoxin alpha (TNF-beta) are pleiotropic cytokines with regulatory functions in inflammatory reactions and T cell activation. Natural TNF inhibitors such as soluble TNF-binding proteins, i.e. TNFsR55 and TNFsR75, are shed from white blood cells and probably other cells. These naturally occurring inhibitors of TNF are shown to be 10 times less effective than the bivalent antagonist of TNF, recombinant soluble TNF receptor p55-human gamma 3 fusion protein (rsTNFR-p55h gamma 3), in controlling the release of prostaglandin E2 (PGE2) and collagenase by fibroblasts, as well as in controlling T cell proliferation. In order to block the action of rhTNF-alpha added to fibroblasts, a fivefold excess of rsTNFR-p55h gamma 3 was sufficient, but concentrations of a hundred to a thousand times higher were required to obtain a significant inhibition of T cell activation. This concentration appears to be required to block membrane-bound TNF-alpha on peripheral blood mononuclear cells as shown by Scatchard analysis. We additionally show that rsTNFR-p55h gamma 3 at high concentrations also blocks T cell activation by dendritic cells. In conclusion rsTNFR-p55h gamma 3 has a much higher anti-inflammatory effect than immunosuppressive effect.
Mots-clé
Antigens, CD/metabolism, Cell Division/drug effects, Cells, Cultured, Collagenases/biosynthesis, Dinoprostone/biosynthesis, Humans, Lymphocyte Activation, Phytohemagglutinins/pharmacology, Receptors, Tumor Necrosis Factor/metabolism, Receptors, Tumor Necrosis Factor, Type I, Recombinant Fusion Proteins/metabolism, Synovial Membrane/cytology, Synovial Membrane/drug effects, T-Lymphocytes/immunology, Tumor Necrosis Factor-alpha/antagonists & inhibitors
Pubmed
Web of science
Création de la notice
19/02/2010 19:40
Dernière modification de la notice
20/08/2019 15:44
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