Please use this identifier to cite or link to this item: https://doi.org/10.1038/ni.3694
Title: Essential role for the transcription factor Bhlhe41 in regulating the development, self-renewal and BCR repertoire of B-1a cells
Authors: Kreslavsky, Taras
Vilagos, Bojan
Tagoh, Hiromi
Poliakova, Daniela Kostanova
Schwickert, Tanja A
Woehner, Miriam
Jaritz, Markus
Weiss, Siegfried
Taneja, Reshma 
Rossner, Moritz J
Busslinger, Meinrad
Keywords: Science & Technology
Life Sciences & Biomedicine
Immunology
CENTER B-CELL
POSITIVE SELECTION
FETAL
EXPRESSION
DISTINCT
SINGLE
MICE
IDENTIFICATION
PROLIFERATION
LYMPHOPOIESIS
Issue Date: 1-Apr-2017
Publisher: NATURE PUBLISHING GROUP
Citation: Kreslavsky, Taras, Vilagos, Bojan, Tagoh, Hiromi, Poliakova, Daniela Kostanova, Schwickert, Tanja A, Woehner, Miriam, Jaritz, Markus, Weiss, Siegfried, Taneja, Reshma, Rossner, Moritz J, Busslinger, Meinrad (2017-04-01). Essential role for the transcription factor Bhlhe41 in regulating the development, self-renewal and BCR repertoire of B-1a cells. NATURE IMMUNOLOGY 18 (4) : 442-+. ScholarBank@NUS Repository. https://doi.org/10.1038/ni.3694
Abstract: © 2017 Nature America, Inc., part of Springer Nature. All rights reserved. Innate-like B-1a cells provide a first line of defense against pathogens, yet little is known about their transcriptional control. Here we identified an essential role for the transcription factor Bhlhe41, with a lesser contribution by Bhlhe40, in controlling B-1a cell differentiation. Bhlhe41-/- Bhlhe40-/- B-1a cells were present at much lower abundance than were their wild-type counterparts. Mutant B-1a cells exhibited an abnormal cell-surface phenotype and altered B cell receptor (BCR) repertoire exemplified by loss of the phosphatidylcholine-specific VH 12V κ4 BCR. Expression of a pre-rearranged VH 12V κ4 BCR failed to 'rescue' the mutant phenotype and revealed enhanced proliferation accompanied by increased cell death. Bhlhe41 directly repressed the expression of cell-cycle regulators and inhibitors of BCR signaling while enabling pro-survival cytokine signaling. Thus, Bhlhe41 controls the development, BCR repertoire and self-renewal of B-1a cells.
Source Title: NATURE IMMUNOLOGY
URI: https://scholarbank.nus.edu.sg/handle/10635/155225
ISSN: 15292908
15292916
DOI: 10.1038/ni.3694
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