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- W2073898186 abstract "The activation of Gs-coupled A2A adenosine receptor on the surface of immune cells increases levels of immunosuppressive cyclic AMP and leads to inhibition of secretion of proinflammatory cytokines, which, in turn, results in downregulation of acute inflammation. The role of A2A receptors in the regulation of inflammation appears to be non-redundant. Small doses of inflammatory stimulus induce high levels of proinflammatory cytokines and extensive tissue injury in A2A receptor-deficient (Adora2a−/−) mice leading to death due to unregulated inflammatory damage. The gene-dose effect of A2A receptor expression in T cells suggests that there are no spare A2A receptors and that the final outcome of immune cell activation may be dependent on the number of these receptors on the individual immune cells. Heterozygous (Adora2a+/−) mice express decreased levels of A2A receptor on the surface and adenosine-induced cAMP-accumulation of immune cells was lower than in wild-type. Thus, the number of A2A receptors determines cAMP response to adenosine and may pre-determine the immunosuppressive role of adenosine. Drug Dev Res 64:172–177, 2005. © 2005 Wiley-Liss, Inc." @default.
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- W2073898186 date "2005-01-01" @default.
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- W2073898186 title "Physiological regulation of acute inflammation by A2A adenosine receptor" @default.
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- W2073898186 doi "https://doi.org/10.1002/ddr.10428" @default.
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