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The aryl hydrocarbon receptor controls cell-fate decisions in B cells.

Journal article
Authors Bharat Vaidyanathan
Ashutosh Chaudhry
William T Yewdell
Davide Angeletti
Wei-Feng Yen
Adam K Wheatley
Christopher A Bradfield
Adrian B McDermott
Jonathan W Yewdell
Alexander Y Rudensky
Jayanta Chaudhuri
Published in The Journal of experimental medicine
Volume 214
Issue 1
Pages 197-208
ISSN 1540-9538
Publication year 2017
Published at
Pages 197-208
Language en
Keywords Animals, B-Lymphocytes, physiology, Cell Differentiation, Cytidine Deaminase, physiology, Female, Immunoglobulin Class Switching, Influenza A Virus, H1N1 Subtype, immunology, Male, Mice, Mice, Inbred C57BL, Plasma Cells, cytology, Polychlorinated Dibenzodioxins, pharmacology, Positive Regulatory Domain I-Binding Factor 1, Receptors, Aryl Hydrocarbon, physiology, T-Lymphocytes, physiology, Transcription Factors, physiology
Subject categories Immunology in the medical area, Immunology


Generation of cellular heterogeneity is an essential feature of the adaptive immune system. This is best exemplified during humoral immune response when an expanding B cell clone assumes multiple cell fates, including class-switched B cells, antibody-secreting plasma cells, and memory B cells. Although each cell type is essential for immunity, their generation must be exquisitely controlled because a class-switched B cell cannot revert back to the parent isotype, and a terminally differentiated plasma cell cannot contribute to the memory pool. In this study, we show that an environmental sensor, the aryl hydrocarbon receptor (AhR) is highly induced upon B cell activation and serves a critical role in regulating activation-induced cell fate outcomes. We find that AhR negatively regulates class-switch recombination ex vivo by altering activation-induced cytidine deaminase expression. We further demonstrate that AhR suppresses class switching in vivo after influenza virus infection and immunization with model antigens. In addition, by regulating Blimp-1 expression via Bach2, AhR represses differentiation of B cells into plasmablasts ex vivo and antibody-secreting plasma cells in vivo. These experiments suggest that AhR serves as a molecular rheostat in B cells to brake the effector response, possibly to facilitate optimal recall responses. Thus, AhR might represent a novel molecular target for manipulation of B cell responses during vaccination.

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