New insights into the regulation of inflammation by adenosine
J. Clin. Invest. Joel Linden, et al. 116:1835 doi:10.1172/JCI29125 [Go to this article.]

Figure 1
Anti- and proinflammatory effects mediated by activation of the A_2B AR. (A) In macrophages, the release of TNF-α and other proinflammatory cytokines is inhibited as a result of activating either the A_2AAR or the A_2BAR. These effects are amplified if TNF-α production is stimulated by LPS, which signals through TLR4 and other Toll-like receptors. Activation of the A_2BAR also stimulates production of the antiinflammatory cytokine IL-10. (B) In endothelial cells and other cells noted in Table 1, activation of the A_2BAR stimulates IL-6 and other proinflammatory cytokines. Hypoxia increases the intracellular production of adenosine, which is transported outside the cell by nucleoside transport proteins. Hypoxia and possibly activation of the A_2BAR stimulate the release of ATP and the production of the A_2BAR and ectoenzymes (CD39 and CD73) that convert ATP to adenosine. Vasodilation in response to A_2BAR activation may increase shear stress to stimulate ATP release.