dc.contributor.authorChng, Song Hui
dc.contributor.authorKundu, Parag
dc.contributor.authorDominguez-Brauer, Carmen
dc.contributor.authorTeo, Wei Ling
dc.contributor.authorKawajiri, Kaname
dc.contributor.authorFujii-Kuriyama, Yoshiaki
dc.contributor.authorMak, Tak Wah
dc.contributor.authorPettersson, Sven
dc.date.accessioned2016-09-21T06:07:46Z
dc.date.available2016-09-21T06:07:46Z
dc.date.issued2016
dc.identifier.citationChng, S. H., Kundu, P., Dominguez-Brauer, C., Teo, W. L., Kawajiri, K., Fujii-Kuriyama, Y., et al. (2016). Ablating the aryl hydrocarbon receptor (AhR) in CD11c+ cells perturbs intestinal epithelium development and intestinal immunity. Scientific Reports, 6, 23820-.en_US
dc.identifier.issn2045-2322en_US
dc.identifier.urihttp://hdl.handle.net/10220/41461
dc.description.abstractDiet and microbiome derived indole derivatives are known to activate the ligand induced transcription factor, the Aryl hydrocarbon Receptor (AhR). While the current understanding of AhR biology has confirmed its role in mucosal lymphocytes, its function in intestinal antigen presenting cells (APCs) is poorly understood. Here, we report that Cre-mediated deletion of AhR in CD11c-expressing cells in C57/BL6 mice is associated with altered intestinal epithelial morphogenesis in vivo. Moreover, when co-cultured with AhR-deficient DCs ex vivo, intestinal organoids showed reduced SRY (sex determining region Y)-box 9 and increased Mucin 2 expression, which correlates with reduced Paneth cells and increased goblet cell differentiation, similar to the data obtained in vivo. Further, characterization of intestinal APC subsets, devoid of AhR, revealed an expression pattern associated with aberrant intrinsic Wnt pathway regulation. At a functional level, the loss of AhR in APCs resulted in a dysfunctional epithelial barrier, associated with a more aggressive chemically induced colitis compared to wild type animals. Our results are consistent with a model whereby the AhR signalling pathway may participate in the regulation of innate immunity through intestinal epithelium development and mucosal immunity.en_US
dc.format.extent14 p.en_US
dc.language.isoenen_US
dc.relation.ispartofseriesScientific Reportsen_US
dc.rights© 2016 The Authors. This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/en_US
dc.subjectInnate immunityen_US
dc.subjectMucosal immunologyen_US
dc.titleAblating the aryl hydrocarbon receptor (AhR) in CD11c+ cells perturbs intestinal epithelium development and intestinal immunityen_US
dc.typeJournal Article
dc.contributor.researchSingapore Centre on Environmental Life Sciences Engineering
dc.contributor.schoolSchool of Biological Sciencesen_US
dc.contributor.schoolLee Kong Chian School of Medicine
dc.identifier.doihttp://dx.doi.org/10.1038/srep23820
dc.description.versionPublished versionen_US


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