Role of G-protein-coupled adenosine receptors in downregulation of inflammation and protection from tissue damage
By A. Ohta, M. Sitkovsky. Nature, 2001
1,297 citations recorded by the source corpus.
Subfields: Cellular and Molecular Neuroscience, Molecular Biology, Physiology
View Paper: https://www.semanticscholar.org/paper/2092e32e1429fddabf44973c1983fddb078efafb
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In Cellular and Molecular Neuroscience
In Molecular Biology
- C. Nathan
- H. Eltzschig
- Jiang-fan Chen
- Alexander Y. Rudensky
- T. Eckle
- R. Medzhitov
- C. Serhan
- Nikolaos G. Frangogiannis
In Physiology
Citations in the corpus
- Ischemia and reperfusion—from mechanism to translation (2011, background): “Pharmacological and genetic studies in mouse models of ischemia and reperfusion have shown that signaling through adenosine receptors is protective; for example, through activation of the adenosine A2A receptor (Adora2a) on inflammatory cell”
- Maintenance of the Foxp3-dependent developmental program in mature regulatory T cells requires continued expression of Foxp3 (2007, background): “CD73 is proposed to be involved in the generation of adenosine by T reg cells, which affords negative regulation of inflammatory responses by engaging A2A receptor”
- Adenosine generation catalyzed by CD39 and CD73 expressed on regulatory T cells mediates immune suppression (2007, background): “effects by binding to adenosine type 1 purinergic G protein–coupled cell surface receptors, which are termed A1, A2a, A2B, and A3. Adenosine is a potent inhibitor of T cell responses (19), and the A2A receptor has been identified as the major antiinflammatory adenosine receptor associated with T cel”
- Points of control in inflammation (2002, background): “Mice deprived of purinergic A2a receptors succumb to normally sublethal doses of microbial and chemical toxin”