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

Artikel i vetenskaplig tidskrift
Författare 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
Publicerad i The Journal of experimental medicine
Volym 214
Nummer/häfte 1
Sidor 197-208
ISSN 1540-9538
Publiceringsår 2017
Publicerad vid
Sidor 197-208
Språk en
Länkar dx.doi.org/10.1084/jem.20160789
www.ncbi.nlm.nih.gov/entrez/query.f...
Ämnesord 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
Ämneskategorier Immunologi inom det medicinska området, Immunologi

Sammanfattning

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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