Role of A2A adenosine receptors in inflammation

✍ Scribed by Gail W. Sullivan; Joel Linden

• Publisher: John Wiley and Sons
• Year: 1998
• Tongue: English
• Weight: 159 KB
• Volume: 45
• Category: Article
• ISSN: 0272-4391
• DOI: 10.1002/(sici)1098-2299(199811/12)45:3/4<103::aid-ddr4>3.0.co;2-w

✦ Synopsis

A 2A adenosine receptors are expressed on immune cells including neutrophils, lymphocytes, eosinophils, monocytes/macrophages, and mast cells. Activation of A 2A receptors on these cells stimulates an increase in [cyclic AMP] i and causes a diminution of inflammatory responses. In mast cells, degranulation is inhibited; in neutrophils, adherence is reduced and the release of reactive oxygen species is inhibited; in monocytes, differentiation to macrophages is inhibited and the release of tumor necrosis factor-α is inhibited; and in lymphocytes, TCR-triggered interleukin-2 α chain (CD25) up-regulation is reduced. In vivo, selective adenosine A 2A agonists decrease inflammation in both infectious and noninfectious models. High concentrations (micromolar) of the A 3 selective agonist, IB-MECA, produce anti-inflammatory responses that are mediated by A 2A receptors. Selective activation of A 2A adenosine receptors with pharmaceutical agents may be a useful strategy for ameliorating an inappropriate and/or an extensive inflammatory response.