Maturation of dendritic cells is accompanied by rapid transcriptional silencing of class II transactivator (CIITA) expression.

Détails

ID Serval
serval:BIB_14EF7F226A0A
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Maturation of dendritic cells is accompanied by rapid transcriptional silencing of class II transactivator (CIITA) expression.
Périodique
The Journal of experimental medicine
Auteur(s)
Landmann S, Mühlethaler-Mottet A, Bernasconi L, Suter T, Waldburger JM, Masternak K, Arrighi JF, Hauser C, Fontana A, Reith W
Statut éditorial
Publié
Date de publication
08/2001
Peer-reviewed
Oui
Langue
anglais
Résumé
Cell surface expression of major histocompatibility complex class II (MHCII) molecules is increased during the maturation of dendritic cells (DCs). This enhances their ability to present antigen and activate naive CD4+ T cells. In contrast to increased cell surface MHCII expression, de novo biosynthesis of MHCII mRNA is turned off during DC maturation. We show here that this is due to a remarkably rapid reduction in the synthesis of class II transactivator (CIITA) mRNA and protein. This reduction in CIITA expression occurs in human monocyte-derived DCs and mouse bone marrow–derived DCs, and is triggered by a variety of different maturation stimuli, including lipopolysaccharide, tumor necrosis factor α, CD40 ligand, interferon α, and infection with Salmonella typhimurium or Sendai virus. It is also observed in vivo in splenic DCs in acute myelin oligodendrocyte glycoprotein induced experimental autoimmune encephalitis. The arrest in CIITA expression is the result of a transcriptional inactivation of the MHC2TA gene. This is mediated by a global repression mechanism implicating histone deacetylation over a large domain spanning the entire MHC2TA regulatory region.
Mots-clé
MHC class II, CIITA, experimental autoimmune encephalitis, bare lymphocyte syndrome, histone deacetylation
Pubmed
Open Access
Oui
Création de la notice
23/03/2020 12:44
Dernière modification de la notice
24/03/2020 7:26
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