期刊
BRITISH JOURNAL OF PHARMACOLOGY
卷 153, 期 -, 页码 S457-S464出版社
WILEY
DOI: 10.1038/bjp.2008.23
关键词
adenosine receptor; T regulatory cells; immunity; cancer; inflammation; lymphocytes; T-cell receptor; infectious diseases; ectonucleotidases
资金
- NCCIH NIH HHS [R21 AT002788, AT002788] Funding Source: Medline
- NCI NIH HHS [CA111985, CA112561, R01 CA111985, R01 CA112561] Funding Source: Medline
- NHLBI NIH HHS [P01 HL076540, R01 HL063972-08, R01 HL063972, R01 HL057307-08, R01 HL057307, HL076540, HL63972] Funding Source: Medline
The intensity and duration of host responses are determined by protective mechanisms that control tissue injury by dampening down inflammation. Adenosine generation and consequent effects, mediated via A2A adenosine receptors (A2AR) on effector cells, play a critical role in the pathophysiological modulation of these responses in vivo. Adenosine is both released by hypoxic cells/tissues and is also generated from extracellular nucleotides by ecto-enzymes e. g. CD39 (ENTPD1) and CD73 that are expressed by the vasculature and immune cells, in particular by T regulatory cell. In general, these adenosinergic mechanisms minimize the extent of collateral damage to host tissues during the course of inflammatory reactions. However, induction of suppressive pathways might also cause escape of pathogens and permit dissemination. In addition, adenosinergic responses may inhibit immune responses while enhancing vascular angiogenic responses to malignant cells that promote tumor growth. Novel drugs that block A2AR-adenosinergic effects and/or adenosine generation have the potential to boost pathogen destruction and to selectively destroy malignant tissues. In the latter instance, future treatment modalities might include novel 'anti-adenosinergic' approaches that augment immune clearance of malignant cells and block permissive angiogenesis. This review addresses several possible pharmacological modalities to block adenosinergic pathways and speculates on their future application together with impacts on human disease.
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