Journal
CURRENT OPINION IN PHARMACOLOGY
Volume 9, Issue 4, Pages 501-506Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.coph.2009.05.005
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Funding
- NCCIH NIH HHS [R21 AT002788-01A1, R21 AT002788] Funding Source: Medline
- NCI NIH HHS [R01 CA111985-01A2, R01 CA112561-01, R01 CA112561, R01 CA111985] Funding Source: Medline
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Hypoxia-driven increase of extracellular adenosine in local tissue microenvironments of inflamed and cancerous tissues plays a critical role in the regulation of tissue destruction by activated immune cells. Accumulated data suggest that injection or consumption of A2A adenosine receptor (A2AR) antagonists may represent a drug treatment that diminishes adenosine-mediated immunosuppression. Since this, in turn, enhances the immune response, inhibition of adenosine-A2AR signaling may be a promising approach to enhance anti-tumor or anti-pathogen immune response. Patients with disorders characterized by excessive inflammation may be at risk to A2AR antagonists (e.g. caffeine) because of the effect to increase inflammatory damage secondary to enhanced immunity. On the other hand, enhancement of hypoxia-adenosinergic immunomodulatory pathways may be beneficial to prevent inflammatory tissue destruction.
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