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      Adenosine inhibits IL-12 and TNF-[alpha] production via adenosine A2a receptor-dependent and independent mechanisms.

      The FASEB Journal
      Adenosine, pharmacology, Animals, Interleukin-10, biosynthesis, Interleukin-12, Lipopolysaccharides, Macrophages, drug effects, Macrophages, Peritoneal, Male, Mice, Mice, Inbred BALB C, Mice, Mutant Strains, Mitogen-Activated Protein Kinases, metabolism, Purinergic P1 Receptor Agonists, Purinergic P1 Receptor Antagonists, Receptor, Adenosine A2A, Receptors, Purinergic P1, deficiency, genetics, Tumor Necrosis Factor-alpha

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          Abstract

          Interleukin 12 (IL-12) is a crucial cytokine in the regulation of T helper 1 vs. T helper 2 immune responses. In the present study, we investigated the effect of the endogenous purine nucleoside adenosine on the production of IL-12. In mouse macrophages, adenosine suppressed IL-12 production. Although the order of potency of adenosine receptor agonists suggested the involvement of A2a receptors, data obtained with A2a receptor-deficient mice showed that the adenosine suppression of IL-12 and even TNF-alpha production is only partly mediated by A2a receptor ligation. Studies with adenosine receptor antagonists or the adenosine uptake blocker dipyridamole showed that adenosine released endogenously also decreases IL-12. Although adenosine increases IL-10 production, the inhibition of IL-12 production is independent of the increased IL-10. The mechanism of action of adenosine was not associated with alterations of the activation of the p38 and p42/p44 mitogen-activated protein kinases or the phosphorylation of the c-Jun terminal kinase. Adenosine failed to affect steady-state levels of either IL-12 p35 or p40 mRNA, but augmented IL-10 mRNA levels. In summary, adenosine inhibits IL-12 production via various adenosine receptors. These results support the notion that adenosine-based therapies might be useful in certain autoimmune and/or inflammatory diseases.

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