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

https://www.ncbi.nlm.nih.gov/pubmed/33844457

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.