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Open AccessArticle

AHR Signaling Dampens Inflammatory Signature in Neonatal Skin γδ T Cells

IUF—Leibniz Research Institute for Environmental Medicine, Auf’m Hennekamp 50, D-40225 Düsseldorf, Germany
Institute of Clinical Chemistry and Laboratory Diagnostic, University of Düsseldorf, Universitätsstrasse 1, D-40225 Düsseldorf, Germany
Immunology and Environment, Life & Medical Sciences (LIMES) Institute, University of Bonn, Carl-Troll-Str. 31, D-53115 Bonn, Germany
Institute of Medical Microbiology, Immunology and Parasitology, University of Bonn, Venusberg Campus 1, D-53127 Bonn, Germany
BMFZ—Genomics & Transcriptomics Laboratory, University of Düsseldorf, Universitätsstrasse 1, D-40225 Düsseldorf, Germany
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2020, 21(6), 2249;
Received: 19 February 2020 / Revised: 19 March 2020 / Accepted: 20 March 2020 / Published: 24 March 2020
(This article belongs to the Special Issue Aryl Hydrocarbon Receptor in Biology and Toxicology 2.0)
Background Aryl hydrocarbon receptor (AHR)-deficient mice do not support the expansion of dendritic epidermal T cells (DETC), a resident immune cell population in the murine epidermis, which immigrates from the fetal thymus to the skin around birth. Material and Methods In order to identify the gene expression changes underlying the DETC disappearance in AHR-deficient mice, we analyzed microarray RNA-profiles of DETC, sorted from the skin of two-week-old AHR-deficient mice and their heterozygous littermates. In vitro studies were done for verification, and IL-10, AHR repressor (AHRR), and c-Kit deficient mice analyzed for DETC frequency. Results We identified 434 annotated differentially expressed genes. Gene set enrichment analysis demonstrated that the expression of genes related to proliferation, ion homeostasis and morphology differed between the two mouse genotypes. Importantly, with 1767 pathways the cluster-group “inflammation” contained the majority of AHR-dependently regulated pathways. The most abundant cluster of differentially expressed genes was “inflammation.” DETC of AHR-deficient mice were inflammatory active and had altered calcium and F-actin levels. Extending the study to the AHRR, an enigmatic modulator of AHR-activity, we found approximately 50% less DETC in AHRR-deficient mice than in wild-type-littermates. Conclusion AHR-signaling in DETC dampens their inflammatory default potential and supports their homeostasis in the skin. View Full-Text
Keywords: γδ T cell; epidermis; aryl hydrocarbon receptor γδ T cell; epidermis; aryl hydrocarbon receptor
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MDPI and ACS Style

Merches, K.; Schiavi, A.; Weighardt, H.; Steinwachs, S.; Teichweyde, N.; Förster, I.; Hochrath, K.; Schumak, B.; Ventura, N.; Petzsch, P.; Köhrer, K.; Esser, C. AHR Signaling Dampens Inflammatory Signature in Neonatal Skin γδ T Cells. Int. J. Mol. Sci. 2020, 21, 2249.

AMA Style

Merches K, Schiavi A, Weighardt H, Steinwachs S, Teichweyde N, Förster I, Hochrath K, Schumak B, Ventura N, Petzsch P, Köhrer K, Esser C. AHR Signaling Dampens Inflammatory Signature in Neonatal Skin γδ T Cells. International Journal of Molecular Sciences. 2020; 21(6):2249.

Chicago/Turabian Style

Merches, Katja; Schiavi, Alfonso; Weighardt, Heike; Steinwachs, Swantje; Teichweyde, Nadine; Förster, Irmgard; Hochrath, Katrin; Schumak, Beatrix; Ventura, Natascia; Petzsch, Patrick; Köhrer, Karl; Esser, Charlotte. 2020. "AHR Signaling Dampens Inflammatory Signature in Neonatal Skin γδ T Cells" Int. J. Mol. Sci. 21, no. 6: 2249.

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