The mechanisms that control the termination of the mammalian inflammatory response in vivo remain unclear. In 20/27 December Nature Akio Ohta & Michail Sitkovsky from National Institutes of Health, Bethesda, USA show that G-protein-coupled A2a adenosine receptors have an essential role in the attenuation of inflammation and tissue damage in vivo.

Ohta & Sitkovsky studied mice deficient in the A2a adenosine receptor and observed that sub-threshold doses of an inflammatory stimulus caused extensive tissue damage, and more prolonged and higher levels of pro-inflammatory cytokines than in the wild-type mice — where the tissue damage was minimal. In addition, three other different models of inflammation as well as bacterial endotoxin-induced septic shock elicited similar results (Nature 2001, 414:916-920).

"The marked effects of A2a receptor deficiency on functions of immune cells in vivo point to the possible role of A2a receptors in the regulation of different stages of...

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