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dc.contributor.authorVaidyanathan, B
dc.contributor.authorChaudhry, A
dc.contributor.authorYewdell, WT
dc.contributor.authorAngeletti, D
dc.contributor.authorYen, W-F
dc.contributor.authorWheatley, AK
dc.contributor.authorBradfield, CA
dc.contributor.authorMcDermott, AB
dc.contributor.authorYewdell, JW
dc.contributor.authorRudensky, AY
dc.contributor.authorChaudhuri, J
dc.date.accessioned2020-12-17T04:38:45Z
dc.date.available2020-12-17T04:38:45Z
dc.date.issued2017-01-01
dc.identifierpii: jem.20160789
dc.identifier.citationVaidyanathan, B., Chaudhry, A., Yewdell, W. T., Angeletti, D., Yen, W. -F., Wheatley, A. K., Bradfield, C. A., McDermott, A. B., Yewdell, J. W., Rudensky, A. Y. & Chaudhuri, J. (2017). The aryl hydrocarbon receptor controls cell-fate decisions in B cells. JOURNAL OF EXPERIMENTAL MEDICINE, 214 (1), pp.197-208. https://doi.org/10.1084/jem.20160789.
dc.identifier.issn0022-1007
dc.identifier.urihttp://hdl.handle.net/11343/255399
dc.description.abstractGeneration 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.
dc.languageEnglish
dc.publisherROCKEFELLER UNIV PRESS
dc.rights.urihttps://creativecommons.org/licenses/by-nc-sa/4.0
dc.titleThe aryl hydrocarbon receptor controls cell-fate decisions in B cells
dc.typeJournal Article
dc.identifier.doi10.1084/jem.20160789
melbourne.affiliation.departmentMicrobiology and Immunology
melbourne.source.titleJournal of Experimental Medicine
melbourne.source.volume214
melbourne.source.issue1
melbourne.source.pages197-208
dc.rights.licenseCC BY-NC-SA
melbourne.elementsid1255523
melbourne.contributor.authorWheatley, Adam
dc.identifier.eissn1540-9538
melbourne.accessrightsOpen Access


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