A(2B) adenosine receptors in immunity and inflammation

• Published in: Trends in immunology 2009-06, Vol.30 (6), p.263-270
• Main Authors: Haskó, György, Csóka, Balázs, Németh, Zoltán H, Vizi, E Sylvester, Pacher, Pál
• Format: Article
• Language: English
• Subjects: Animals; Antigen Presentation; Asthma - etiology; Asthma - metabolism; Colitis - etiology; Colitis - metabolism; Endothelial Cells - immunology; Feedback, Physiological; Humans; Immunologic Factors - genetics; Immunologic Factors - immunology; Immunologic Factors - metabolism; Inflammation Mediators - immunology; Inflammation Mediators - metabolism; Mast Cells - immunology; Mast Cells - metabolism; Mast Cells - pathology; Neovascularization, Pathologic - immunology; Neovascularization, Pathologic - metabolism; Neovascularization, Physiologic - immunology; Receptor, Adenosine A2B - genetics; Receptor, Adenosine A2B - immunology; Receptor, Adenosine A2B - metabolism
• ISSN: 1471-4981
• DOI: 10.1016/j.it.2009.04.001

A(2B) adenosine receptors are increasingly recognized as important orchestrators of inflammation. A(2B) receptor activation promotes the inflammatory response of mast cells, epithelial cells, smooth muscle cells and fibroblasts, thereby contributing to the pathophysiology of asthma and colitis. A(2B) receptor stimulation limits endothelial cell inflammatory responses and permeability and suppresses macrophage activation thereby preventing tissue injury after episodes of hypoxia and ischemia. A(2B) receptor stimulation also promotes the production of angiogenic cytokines by endothelial cells, mast cells and dendritic cells, aiding granuloma tissue formation and inflammatory resolution, but can also contribute to tumor growth. A(2B) receptors are, thus, potentially important pharmacological targets in treating immune system dysfunction and inflammation.