ArticleThe Journal of investigative dermatology2015
Activation of the arylhydrocarbon receptor causes immunosuppression primarily by modulating dendritic cells.
Article in The Journal of investigative dermatology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
27 citing papers in PubMed, 53 citations in OpenAlex.
- Aryl hydrocarbon receptor pharmacology-mechanisms, ligands, and therapeutic potential.Pharmacological reviews · 2026Review
- Melatonin Regulates Arylhydrocarbon Receptor Mediated UVR-Induced Processes Related to Inflammation, Skin Aging and Carcinogenesis in Human Ex Vivo Skin.Experimental dermatology · 2026Article
- AhR signaling in skin-resident CD207Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- The aryl hydrocarbon receptor controls IFN-γ-induced immune checkpoints PD-L1 and IDO via the JAK/STAT pathway in lung adenocarcinoma.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Targeting aryl hydrocarbon receptor functionally restores tolerogenic dendritic cells derived from patients with multiple sclerosis.The Journal of clinical investigation · 2024Article
- The Aryl Hydrocarbon Receptor Controls IFNγ-Induced Immune Checkpoints PD-L1 and IDO via the JAK/STAT Pathway in Lung Adenocarcinoma.bioRxiv : the preprint server for biology · 2024Article
- The Antioxidant PAPLAL Protects against Allergic Contact Dermatitis in Experimental Models.Antioxidants (Basel, Switzerland) · 2024Article
- The Aryl Hydrocarbon Receptor: Impact on the Tumor Immune Microenvironment and Modulation as a Potential Therapy.Cancers · 2024Review
- Immunomodulatory effects of nanoparticles on dendritic cells in a model of allergic contact dermatitis: importance of PD-L2 expression.Scientific reports · 2023Article
- Immunomodulatory Effects of Nanoparticles on Dendritic Cells in a Model of Allergic Contact Dermatitis - Importance of PD-L2 Expression.Research square · 2023Article
- Review
- Photoaging: UV radiation-induced inflammation and immunosuppression accelerate the aging process in the skin.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022Review
- Review
- Inferred Causal Mechanisms of Persistent FMDV Infection in Cattle from Differential Gene Expression in the Nasopharyngeal Mucosa.Pathogens (Basel, Switzerland) · 2022Article
- The Aryl Hydrocarbon Receptor in the Pathogenesis of Environmentally-Induced Squamous Cell Carcinomas of the Skin.Frontiers in oncology · 2022Review
- Recent advances in the development of AHR antagonists in immuno-oncology.RSC medicinal chemistry · 2021Review
- Trajectory Shifts in Interdisciplinary Research of the Aryl Hydrocarbon Receptor-A Personal Perspective on Thymus and Skin.International journal of molecular sciences · 2021Review
- Microbiota-Mediated Immune Regulation in Atherosclerosis.Molecules (Basel, Switzerland) · 2021Review
- DNA Damage Response and Immune Defense.International journal of molecular sciences · 2020Review
- Frontal Fibrosing Alopecia. An Example of Disrupted Aryl Hydrocarbon Receptor-Mediated Immunological Homeostasis in the Skin?Clinical, cosmetic and investigational dermatology · 2020Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
UVR suppresses the immune system in an antigen-specific manner via induction of regulatory T cells (Tregs). The specific immunosuppression by UVR harbors therapeutic potential but is associated with UVR-induced DNA damage, requiring the identification of other triggers inducing the same immunosuppressive effects without DNA damage. The aryl hydrocarbon receptor (AhR) was identified as a molecular target for UVR and its activation to be involved in UVR-induced immunosuppression. Accordingly, the AhR agonist 4-n-nonylphenol (NP) suppressed sensitization and induced Treg similar to UVR. Here we show that antigen-presenting cells are critically involved in AhR-induced immunosuppression. Injection of hapten-coupled dendritic cells (DCs) treated with NP into mice did not result in sensitization but induced Treg. NP induced the release of IL-2 by DC that subsequently triggered the release of IL-10. NP upregulated the negative regulatory molecule B7-H4 via the release of IL-2 that was functionally relevant as inhibition of B7-H4 prevented the induction of Treg. Together, this indicates that activation of the AhR switches antigen-presenting cells from a stimulatory into a regulatory phenotype, ultimately inducing Treg. Thus, AhR agonists may represent an alternative to suppress the immune system like UVR but without causing the adverse effects of UVR including DNA damage.
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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.