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Role of A 2A adenosine receptors in inflammation
Author(s) -
Sullivan Gail W.,
Linden Joel
Publication year - 1998
Publication title -
drug development research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.582
H-Index - 60
eISSN - 1098-2299
pISSN - 0272-4391
DOI - 10.1002/(sici)1098-2299(199811/12)45:3/4<103::aid-ddr4>3.0.co;2-w
Subject(s) - receptor , inflammation , degranulation , adenosine , tumor necrosis factor alpha , chemistry , adenosine receptor , adenosine a2a receptor , immune system , agonist , cytokine , pharmacology , immunology , microbiology and biotechnology , biology , biochemistry
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. Drug Dev. Res. 45:103–112, 1998. © 1998 Wiley‐Liss, Inc.