ArticleInternational journal of molecular sciences2020
AHR Signaling Dampens Inflammatory Signature in Neonatal Skin γδ T Cells.
Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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The trial behind it
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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
- The aryl hydrocarbon receptor: structure, signaling, physiology and pathology.Signal transduction and targeted therapy · 2026Review
- Reflections on the gamma delta T cell conference in Toronto 2025 - human therapies, mouse models and white elephants in the room.EXCLI journal · 2025Article
- γδ T cells in diabetes mellitus: dual roles and therapeutic implications.Frontiers in immunology · 2025Review
- Cell Cultures as a Versatile Tool in the Research and Treatment of Autoimmune Connective Tissue Diseases.Cells · 2023Review
- γδ T Cells and Allergic Diseases.Clinical reviews in allergy & immunology · 2023Review
- The Ah Receptor from Toxicity to Therapeutics: Report from the 5th AHR Meeting at Penn State University, USA, June 2022.International journal of molecular sciences · 2023Article
- Inhibition of aryl hydrocarbon receptor signaling promotes the terminal differentiation of human erythroblasts.Journal of molecular cell biology · 2022Article
- The aryl hydrocarbon receptor at the forefront of host-microbe interactions in the skin: A perspective on current knowledge gaps and directions for future research and therapeutic applications.Experimental dermatology · 2021Article
- The molecular mechanisms supporting the homeostasis and activation of dendritic epidermal T cell and its role in promoting wound healing.Burns & trauma · 2021Review
- Skin Resident γδ T Cell Function and Regulation in Wound Repair.International journal of molecular sciences · 2020Review
- Epigenetic Regulations of AhR in the Aspect of Immunomodulation.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.