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CD73 is a cell surface enzyme of the purine catabolic pathway that catalyzes the breakdown of AMP to adenosine. Because of the strong immunosuppressive and antiinflammatory properties of adenosine, we predicted that cd73^−/− mice would develop severe experimental autoimmune encephalomyelitis (EAE), an animal model for the central nervous system (CNS) inflammatory disease, multiple sclerosis. Surprisingly, cd73^−/− mice were resistant to EAE. However, CD4 T cells from cd73^−/− mice secreted more proinflammatory cytokines than wild-type (WT) mice and were able to induce EAE when transferred into naïve cd73^+/+ T cell-deficient recipients. Therefore, the protection from EAE observed in cd73^−/− mice was not caused by a deficiency in T cell responsiveness. Immunohistochemistry showed that cd73^−/− mice had fewer infiltrating lymphocytes in their CNS compared with WT mice. Importantly …