Titre
Mechanism of cyclosporin A-induced immunosuppression. Cyclosporin A inhibits receptor-mediated and non-receptor-mediated lymphokine production as well as interleukin-2-induced proliferation in cloned T lymphocytes
Type
article
Institution
UNIL/CHUV/Unisanté + institutions partenaires
Périodique
Auteur(s)
Harris, D. T.
Auteure/Auteur
Kozumbo, W. J.
Auteure/Auteur
Cerutti, P. A.
Auteure/Auteur
Cerottini, J. C.
Auteure/Auteur
Liens vers les personnes
Liens vers les unités
ISSN
0008-8749
Statut éditorial
Publié
Date de publication
1987-10
Volume
109
Numéro
1
Première page
104
Dernière page/numéro d’article
14
Notes
Journal Article --- Old month value: Oct 1
Résumé
The effects of cyclosporin A (CyA) on the activation processes of cloned murine cytotoxic T lymphocytes (CTL) have been examined. With the use of Day 7 resting cloned CTL it was possible to separate the functions of lymphokine production (macrophage-activating factor, MAF) and interleukin 2 (IL-2)-induced proliferation of these cells. The effect of CyA on each of these activities was analyzed independently. CyA was found to inhibit both receptor-mediated MAF production in response to stimulation with antigen and lectin and MAF production in response to non-receptor-mediated stimulation (by anti-Thy-1 antibodies, ionophore, and phorbol ester). Further, CyA was observed to inhibit the re-entry of these resting CTL into the cell cycle upon stimulation with IL-2. The effect of CyA on MAF production did not appear to be due to inhibition of the signal-transducing mechanism involved in this process (i.e., inositol lipid hydrolysis, calcium mobilization, and protein phosphorylation). The action of CyA on the IL-2-induced proliferation was not due to inhibition of IL-2 receptor expression or the binding of IL-2 to its receptor. Thus, CyA appeared to mediate its suppressive effects on MAF production and IL-2-induced proliferation through an action on some later step(s) in the signal pathways of these activities.
Sujets
PID Serval
serval:BIB_5A74B04D9DD4
PMID
Date de création
2008-01-28T10:14:26.560Z
Date de création dans IRIS
2025-05-20T18:31:13Z