Fiche publication
Date publication
mai 2016
Journal
Cell death and differentiation
Auteurs
Membres identifiés du Cancéropôle Est :
Pr MULLER Sylviane
,
Dr GROS Frédéric
Tous les auteurs :
Arnold J, Murera D, Arbogast F, Fauny JD, Muller S, Gros F
Lien Pubmed
Résumé
To gain new insight into the role of B-cell autophagy, we generated two novel mouse models deficient for the autophagy-related gene (Atg)5, one from the outset pro-B cell stage (Atg5(f/-) Mb1 cre) and the other in mature B cells only (Atg5(f/-) CD21 cre). We show that autophagy is dispensable for pro- to pre-B cell transition, but necessary at a basal level to maintain normal numbers of peripheral B cells. It appears non-essential for B-cell activation under B-cell receptor stimulation but required for their survival after lipopolysaccharide stimulation that drives plasmablast differentiation and for specific IgM production after immunization. Results obtained using Atg5(f/-) CD21 cre × C57BL/6(lpr/lpr) autoimmune-prone mice show that B-cell autophagy is involved in the maintenance of anti-nuclear antibody secretion, elevated number of long-lived plasma cells, and sustains IgG deposits in the kidneys. Thus, treatments specifically targeting autophagy might be beneficial in systemic autoimmune diseases.
Mots clés
Animals, Autoimmunity, immunology, Autophagy, immunology, B-Lymphocytes, immunology, Cells, Cultured, Mice, Mice, Inbred C57BL
Référence
Cell Death Differ.. 2016 May;23(5):853-64
