ArticleBritish journal of pharmacology2009
In vitro induction of T cells that are resistant to A2 adenosine receptor-mediated immunosuppression.
Article in British journal of pharmacology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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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
17 citing papers in PubMed, 25 citations in OpenAlex.
- Inversed Ratio of CD39/CD73 Expression on γδ T Cells in HIV Versus Healthy Controls Correlates With Immune Activation and Disease Progression.Frontiers in immunology · 2022Article
- Antihypoxic oxygenation agents with respiratory hyperoxia to improve cancer immunotherapy.The Journal of clinical investigation · 2020Review
- Inhibition of the Adenosinergic Pathway in Cancer Rejuvenates Innate and Adaptive Immunity.International journal of molecular sciences · 2019Review
- Adenosine A2A Receptor Stimulation Inhibits TCR-Induced Notch1 Activation in CD8+T-Cells.Frontiers in immunology · 2019Article
- AJournal of immunology (Baltimore, Md. : 1950) · 2018Article
- Purinergic regulation of the immune system.Nature reviews. Immunology · 2016Review
- CAR T-cell immunotherapy: The path from the by-road to the freeway?Molecular oncology · 2015Review
- Hostile, hypoxia-A2-adenosinergic tumor biology as the next barrier to overcome for tumor immunologists.Cancer immunology research · 2014Review
- Extracellular adenosine controls NKT-cell-dependent hepatitis induction.European journal of immunology · 2014Article
- Hypoxia-induced and A2A adenosine receptor-independent T-cell suppression is short lived and easily reversible.International immunology · 2014Article
- Antiproliferative effects of selective adenosine receptor agonists and antagonists on human lymphocytes: evidence for receptor-independent mechanisms.Purinergic signalling · 2013Article
- Modulation of G protein-coupled adenosine receptors by strategically functionalized agonists and antagonists immobilized on gold nanoparticles.Purinergic signalling · 2013Article
- Targeting the hypoxia-adenosinergic signaling pathway to improve the adoptive immunotherapy of cancer.Journal of molecular medicine (Berlin, Germany) · 2013Review
- Beyond the antigen receptor: editing the genome of T-cells for cancer adoptive cellular therapies.Frontiers in immunology · 2013Article
- Immunological alterations mediated by adenosine during host-microbial interactions.Immunologic research · 2011Review
- Molecular probes for the A2A adenosine receptor based on a pyrazolo[4,3-e][1,2,4]triazolo[1,5-c]pyrimidin-5-amine scaffold.Bioorganic & medicinal chemistry letters · 2011Article
- Receptor desensitization and blockade of the suppressive effects of prostaglandin E(2) and adenosine on the cytotoxic activity of human melanoma-infiltrating T lymphocytes.Cancer immunology, immunotherapy : CII · 2011Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
background and purposeThe increased levels of extracellular adenosine in inflamed tissues down-regulate activated immune cells via the A(2A) adenosine receptor. This A(2A) adenosine receptor-mediated immunosuppression is a disqualifying obstacle in cancer immunotherapy as it protects cancerous tissues from adoptively transferred anti-tumour T cells. The aim of this study was to test whether the negative selection of T cells will produce T cells that are resistant to inhibition by extracellular adenosine. EXPERIMENTAL APPROACH: Cytotoxic T lymphocytes (CTL) were developed by mixed lymphocyte culture in the presence or absence of the adenosine receptor agonist 5'-N-ethylcarboxamidoadenosine (NECA). The sensitivity of CTL to adenosine analogues was characterized by cAMP induction, interferon-gamma production and cytotoxicity. KEY
resultsCTL that could proliferate even in the presence of NECA were less susceptible to inhibition by A(2A) adenosine receptor agonists, as shown by a much smaller accumulation of cAMP and less inhibition of interferon-gamma production compared with control CTL. The successful protocol to produce CTL that are both resistant to adenosine-mediated immunosuppression and maintain strong cytotoxicity and interferon-gamma secretion required NECA to be added only during the expansion stage after the establishment of CTL. In contrast, the priming of resting T cells in the presence of NECA resulted in T cells with impaired effector functions. CONCLUSIONS AND IMPLICATIONS: Adenosine-resistant effector T cells were successfully obtained by exposure of activated T cells to NECA. These in vitro studies form the basis for future attempts to produce anti-tumour T cells that are more effective in adoptive immunotherapy.
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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.