Glucocorticoid-induced MIF expression by human CEM T cells.
Détails
Télécharger: BIB_DB9CCAFA5DD3.P001.pdf (1238.57 [Ko])
Etat: Public
Version: de l'auteur⸱e
Etat: Public
Version: de l'auteur⸱e
ID Serval
serval:BIB_DB9CCAFA5DD3
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Glucocorticoid-induced MIF expression by human CEM T cells.
Périodique
Cytokine
ISSN
1043-4666
Statut éditorial
Publié
Date de publication
2009
Peer-reviewed
Oui
Volume
48
Numéro
3
Pages
177-185
Langue
anglais
Résumé
Macrophage migration inhibitory factor (MIF) is an upstream activator of the immune response that counter-regulates the immunosuppressive effects of glucocorticoids. While MIF is released by cells in response to diverse microbial and invasive stimuli, evidence that glucocorticoids in low concentrations also induce MIF secretion suggests an additional regulatory relationship between these mediators. We investigated the expression of MIF from the human CEM T cell line, which exists in two well-characterized, glucocorticoid-sensitive (CEM-C7) and glucocorticoid-resistant (CEM-C1) variant clones. Dexamethasone in low concentrations induced MIF secretion from CEM-C7 but not CEM-C1 T cells by a bell-shaped dose response that was similar to that reported previously for the release of MIF by monocytes/macrophages. Glucocorticoid stimulation of CEM-C7 T cells was accompanied by an MIF transcriptional response, which by promoter analysis was found to involve the GRE and ATF/CRE transcription factor binding sites. These data support a glucocorticoid-mediated MIF secretion response by T cells that may contribute to the regulation of the adaptive immune response.
Mots-clé
Glucocorticoid receptor, Inflammation, T cell, Promoter, Migration-Inhibitory Factor, Protein-Kinase Phosphatase-1, Innate Immune-Responses, Rheumatoid-Arthritis, Regulatory Role, Receptor Complex, Septic Shock, Cytokine Mif, Macrophage, Gene
Pubmed
Web of science
Open Access
Oui
Création de la notice
06/08/2009 10:48
Dernière modification de la notice
20/08/2019 16:00