ArticlePloS one2015
An A2B Adenosine Receptor Agonist Promotes Th17 Autoimmune Responses in Experimental Autoimmune Uveitis (EAU) via Dendritic Cell Activation.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 35 citations in OpenAlex.
- Purinergic Receptors in Dendritic Cells.Journal of inflammation research · 2025Review
- Adenosine and Its Receptors in the Pathogenesis and Treatment of Inflammatory Skin Diseases.International journal of molecular sciences · 2024Review
- The Role of Adenosine in γδ T-Cell Regulation of Th17 Responses in Experimental Autoimmune Uveitis.Biomolecules · 2023Review
- Transcriptome network analysis implicates CX3CR1-positive type 3 dendritic cells in non-infectious uveitis.eLife · 2023Article
- The resurgence of the Adora2b receptor as an immunotherapeutic target in pancreatic cancer.Frontiers in immunology · 2023Review
- Upregulated adenosine 2A receptor accelerates post-infectious irritable bowel syndrome by promoting CD4+ T cells' T helper 17 polarization.World journal of gastroenterology · 2022Article
- γδ T Cells Activated in Different Inflammatory Environments Are Functionally Distinct.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- Augmented Th17-stimulating activity of BMDCs as a result of reciprocal interaction between γδ and dendritic cells.Molecular immunology · 2021Article
- Adenosine Signaling in Autoimmune Disorders.Pharmaceuticals (Basel, Switzerland) · 2020Review
- The yin and yang functions of extracellular ATP and adenosine in tumor immunity.Cancer cell international · 2020Review
- The Purinergic System as a Pharmacological Target for the Treatment of Immune-Mediated Inflammatory Diseases.Pharmacological reviews · 2019Review
- The Role of Extracellular Adenosine Generation in the Development of Autoimmune Diseases.Mediators of inflammation · 2018Review
- Interaction between saliva's adenosine and tick parasitism: effects on feeding and reproduction.Parasites & vectors · 2017Article
- Pathological overproduction: the bad side of adenosine.British journal of pharmacology · 2017Review
- Functional Conversion and Dominance of γδ T Subset in Mouse Experimental Autoimmune Uveitis.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- Adenosine and adenosine receptors in the pathogenesis and treatment of rheumatic diseases.Nature reviews. Rheumatology · 2017Review
- The role of adenosinergic pathway in human autoimmune diseases.Immunologic research · 2016Review
- Regulation of Adenosine Deaminase on Induced Mouse Experimental Autoimmune Uveitis.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Blockade of Extracellular ATP Effect by Oxidized ATP Effectively Mitigated Induced Mouse Experimental Autoimmune Uveitis (EAU).PloS one · 2016Article
- CD73 Expressed on γδ T Cells Shapes Their Regulatory Effect in Experimental Autoimmune Uveitis.PloS one · 2016Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
We have recently reported that, although adenosine receptor (AR) agonists have a suppressive effect on Th1 autoreactive T cells, their effect on Th17 autoreactive T cells and γδ T cells is stimulatory and this effect is mainly mediated via A2A adenosine receptors (A2ARs). In this study, we further demonstrate that treatment of C57BL/6 (B6) mice with a selective A2B adenosine receptor (A2BR) agonist greatly enhanced the development of experimental autoimmune uveitis (EAU), whereas treatment with an A2BR antagonist significantly ameliorated severity of EAU. The A2BR agonist-treated mice showed augmented Th17, but not Th1, responses. Mechanistic studies showed that the A2BR agonist-induced enhancement of the Th17 response was significantly lower when TCR-δ-/- mice received the same treatment and that transfer of γδ T cells into TCR-δ-/- mice partially restored this effect. We also showed that dendritic cells (DCs) from A2BR agonist-treated mice showed a significantly increased ability to activate γδ T cells and Th17 autoreactive T cells. Thus, our previous studies have shown that, in EAU, activated γδ T cells possess greatly increased ability to enhance Th17 autoimmune responses. In the present study, we showed that exposure of DCs to A2BR agonist facilitated γδ T cell activation, leading to augmented Th17 responses and progressive EAU development. Our results further support our previous finding that AR agonists have distinct effects on Th1 and Th17 autoimmune responses.
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