ICBP90 Regulates MIF Expression, Glucocorticoid Sensitivity, and Apoptosis at the , MIF Immune Susceptibility Locus.
Fiche publication
Date publication
avril 2021
Journal
Arthritis & rheumatology (Hoboken, N.J.)
Auteurs
Membres identifiés du Cancéropôle Est :
Dr BRONNER Christian
Tous les auteurs :
Yao J, Leng L, Fu W, Li J, Bronner C, Bucala R
Lien Pubmed
Résumé
Macrophage migration inhibitory factor (MIF) is an inflammatory and neurorendocrine mediator that counter-regulates glucocorticoid immunosuppression. MIF polymorphisms, which comprise a variant promoter microsatellite (-794 CATT ), are linked genetically to autoimmune disease severity and to glucocorticoid resistance. While invasive stimuli increase MIF expression, MIF also is upregulated by glucocorticoids, which serves as a physiologic regulator of the inflammatory responses. This study defined interactions between the MIF promoter, the glucocorticoid receptor (GR), and the transcription factor ICBP90, which binds to the promoter in a -794 CATT -length dependent manner, to regulate MIF transcription.
Mots clés
ICBP90, genetic susceptibility, glucocorticoid resistance, glucocorticoids, macrophage migration inhibitory factor
Référence
Arthritis Rheumatol. 2021 Apr 12;: