Thompson Linda F, Takedachi Masahide, Ebisuno Yukihiko, Tanaka Toshiyuki, Miyasaka Masayuki, Mills Jeffery H, Bynoe Margaret S
Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma 73104, USA.
Nucleosides Nucleotides Nucleic Acids. 2008 Jun;27(6):755-60. doi: 10.1080/15257770802145678.
CD73-deficient mice are valuable for evaluating the ability of CD73-generated adenosine to modulate adenosine receptor-mediated responses. Here we report the role of CD73 in regulating lymphocyte migration across two distinct barriers. In the first case, CD73-generated adenosine restricts the migration of lymphocytes across high endothelial venules (HEV) into draining lymph nodes after an inflammatory stimulus, apparently by triggering A(2B) receptors on HEV. Secondly, CD73 promotes the migration of pathogenic T cells into the central nervous system during experimental autoimmune encephalomyelitis. Experiments are in progress to determine whether this effect is also adenosine receptor-mediated and to identify the relevant adenosine receptor.
CD73基因缺陷型小鼠对于评估由CD73生成的腺苷调节腺苷受体介导反应的能力很有价值。在此，我们报告了CD73在调节淋巴细胞穿越两种不同屏障迁移过程中的作用。在第一种情况下，由CD73生成的腺苷明显通过触发高内皮微静脉（HEV）上的A(2B)受体，限制炎症刺激后淋巴细胞穿越HEV迁移至引流淋巴结。其次，在实验性自身免疫性脑脊髓炎期间，CD73促进致病性T细胞迁移至中枢神经系统。目前正在进行实验以确定这种效应是否也是由腺苷受体介导的，并确定相关的腺苷受体。
