ArticlePloS one2012
Adoptive immunotherapy with Cl-IB-MECA-treated CD8+ T cells reduces melanoma growth in mice.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 25 citations in OpenAlex.
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- Istradefylline modulates purinergic enzymes and reduces malignancy-associated factors in B16F10 melanoma cells.Purinergic signalling · 2023Article
- Cancer biology and molecular genetics of AOncogene · 2022Review
- A Novel Antagonistic CD73 Antibody for Inhibition of the Immunosuppressive Adenosine Pathway.Molecular cancer therapeutics · 2021Article
- AFrontiers in oncology · 2021Article
- Targeting Adenosine Receptor Signaling in Cancer Immunotherapy.International journal of molecular sciences · 2018Review
- AMedicinal research reviews · 2018Review
- Role of intracellular and extracellular annexin A1 in migration and invasion of human pancreatic carcinoma cells.BMC cancer · 2014Article
- Adenosine limits the therapeutic effectiveness of anti-CTLA4 mAb in a mouse melanoma model.American journal of cancer research · 2014Article
- Blockade of A2b adenosine receptor reduces tumor growth and immune suppression mediated by myeloid-derived suppressor cells in a mouse model of melanoma.Neoplasia (New York, N.Y.) · 2013Article
- Trial Watch: Adoptive cell transfer for anticancer immunotherapy.Oncoimmunology · 2013Article
- Adenosine receptors as drug targets--what are the challenges?Nature reviews. Drug discovery · 2013Review
- The adenosinergic system in cancer: Key therapeutic target.Oncoimmunology · 2013Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cl-IB-MECA is a selective A3 adenosine receptor agonist, which plays a crucial role in limiting tumor progression. In mice, Cl-IB-MECA administration enhances the anti-tumor T cell-mediated response. However, little is known about the activity of Cl-IB-MECA on CD8+ T cells. The aim of this study was to investigate the effect of ex vivo Cl-IB-MECA treatment of CD8+ T cells, adoptively transferred in melanoma-bearing mice. Adoptive transfer of Cl-IB-MECA-treated CD8+ T cells or a single administration of Cl-IB-MECA (20 ng/mouse) inhibited tumor growth compared with the control group and significantly improved mouse survival. This was associated with the release of Th1-type cytokines and a greater influx of mature Langerin+ dendritic cells (LCs) into the tumor microenvironment. CD8+ T cells treated with Cl-IB-MECA released TNF-α which plays a critical role in the therapeutic efficacy of these cells when injected to mice. Indeed, neutralization of TNF-α by a specific monoclonal Ab significantly blocked the anti-tumor activity of Cl-IB-MECA-treated T cells. This was due to the reduction in levels of cytotoxic cytokines and the presence of fewer LCs. In conclusion, these studies reveal that ex vivo treatment with Cl-IB-MECA improves CD8+ T cell adoptive immunotherapy for melanoma in a TNF-α-dependent manner.
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