A2A adenosine receptor protects tumors from antitumor T cells
By A. Ohta, E. Gorelik, S. Prasad, F. Ronchese, D. Lukashev, M. Wong, Xiaojun Huang, Sheila Caldwell, Kebin Liu, Patrick T. Smith and 5 more. Proceedings of the National Academy of Sciences of the United States of America, 2006
1,017 citations recorded by the source corpus.
Subfields: Immunology, Oncology, Physiology
View Paper: https://www.semanticscholar.org/paper/6206d9b8dcfc5f9d49245e1a1d6c44b4212afbe4
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Citations in the corpus
- Increased Level of Extracellular ATP at Tumor Sites: In Vivo Imaging with Plasma Membrane Luciferase (2008, background): “Recent data show that solid tumours have a gradient of adenosine concentration from the centre to the periphery, higher than the surrounding healthy tissue [6].”
- Adenosine, an endogenous distress signal, modulates tissue damage and repair (2007, background): “This fact combined with the known ability of adenosine to reduce IFNg production via A2A (and A2B) receptors provided a good explanation for the altered tumor growth.(68) Another contributing factor, which was covered before, is that A2A receptors are involved in angiogenesis.”
- Adenosine generation catalyzed by CD39 and CD73 expressed on regulatory T cells mediates immune suppression (2007, background): “Modulation of infl ammation by adenosinergic mechanisms has been rigorously tested in models of T cell–dependent autoimmune and viral hepatitis (21) and in antitumor T cell immunity (22).”
- Immunity, inflammation and cancer: a leading role for adenosine (2013, neutral): “APCP, adenosine 5ʹ-(α,β-methylene) diphosphate; ARL67156, 6-N,N-diethyl-D-β,γ dibromomethylene A TP; Cl-IB-MECA, 1-[2-chloro-6-[[(3-iodophenyl)methyl]amino]9H-purin-9-yl]-1-deoxy-N-methyl-β-D-ribofu ranuronamide; CTLA4, cytotoxic T lymphocyte-associated antigen 4; IB-MECA,1-deoxy-1-[6-[[(3-iodopheny”
- Hypoxic microenvironment in cancer: molecular mechanisms and therapeutic interventions (2023, background): “Hyperoxia treatment suppressed the expressions of adenosine, an immunosuppressive factor,(235) and reactive nitrogen production,(236) and increased IFN-γ levels and perforin granules.(237) Sustained hypoxic stimulation induces mitochondrial stress, resulting in the loss of mitochondrial functions, e”