D3 Article in a professional conference publication
Spontaneous acquisition of plasma cell phenotype in DT40 B cells with inactivation of Bcl-6
Authors: Alinikula J, Mustonen L, Nera KP, Lassila O
Editors: Sirpa Jalkanen, Jaan Lindgren
Conference name: Scandinavian Society for Immunology 37th Annual Meeting
Publisher: BLACKWELL PUBLISHING
Publication year: 2007
Journal: Scandinavian Journal of Immunology
Book title : Scandinavian Journal of Immunology
Journal name in source: SCANDINAVIAN JOURNAL OF IMMUNOLOGY
Journal acronym: SCAND J IMMUNOL
Volume: 65
Issue: 6
First page : 591
Last page: 591
Number of pages: 1
ISSN: 0300-9475
Abstract
B-cell lymphoma 6 (Bcl-6) is implicated in diffuse large cell lymphoma generation, where chromosomal transloca-tions result in constitutive expression of the gene. Bcl-6 is highly expressed in germinal center cells, but the pro-tein is virtually absent in resting B-cells. Gene targeting studies in mice have revealed the necessity of Bcl-6 forgerminal center formation. Mitogenic signaling in B cells induces Bcl-6 production that is needed to keep prdm1,the gene encoding Blimp-1, and subsequent plasma cell differentiation repressed. Our previo us studies haveshown that Pax5 represses plasma cell differentiation and maintains Bcl-6 mRNA expression. We targeted theN-terminal half of the Bcl-6 gene in DT40 cell line to obtain Bcl-6 knockout cells. We found that Bcl-6 repres-ses prdm1 and that the expression of genes encoding proteins of secretory machinery is upregulated in theabsenc e of Bcl-6. The Bcl-6 was found to be needed also for maintenance of Pax5 and AID expression in thesecells. The results suggest that loss of Bcl-6 promotes plasma cell differentiation in the absence of external stimuli.
B-cell lymphoma 6 (Bcl-6) is implicated in diffuse large cell lymphoma generation, where chromosomal transloca-tions result in constitutive expression of the gene. Bcl-6 is highly expressed in germinal center cells, but the pro-tein is virtually absent in resting B-cells. Gene targeting studies in mice have revealed the necessity of Bcl-6 forgerminal center formation. Mitogenic signaling in B cells induces Bcl-6 production that is needed to keep prdm1,the gene encoding Blimp-1, and subsequent plasma cell differentiation repressed. Our previo us studies haveshown that Pax5 represses plasma cell differentiation and maintains Bcl-6 mRNA expression. We targeted theN-terminal half of the Bcl-6 gene in DT40 cell line to obtain Bcl-6 knockout cells. We found that Bcl-6 repres-ses prdm1 and that the expression of genes encoding proteins of secretory machinery is upregulated in theabsenc e of Bcl-6. The Bcl-6 was found to be needed also for maintenance of Pax5 and AID expression in thesecells. The results suggest that loss of Bcl-6 promotes plasma cell differentiation in the absence of external stimuli.
UTU Research Portal