Regulation of dendritic cell trafficking by the ADP-ribosyl cyclase CD38:: Impact on the development of humoral immunity
Regulation of dendritic cell trafficking by the ADP-ribosyl cyclase CD38:: Impact on the development of humoral immunity
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DOI：
10.1016/s1074-7613(04)00048-2
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发表时间：
2004-03-01
期刊：
影响因子：
32.4
通讯作者：
Lund, FE
中科院分区：
文献类型：
--
作者：
Partida-Sánchez, S;Goodrich, S;Lund, FE
缺乏 CD38（一种产生钙动员代谢物 cADPR 的胞外酶）的小鼠会降低 T 细胞依赖性抗体反应。尽管预期 CD38 在 B 细胞激活中发挥作用，但我们发现 CD38 调节树突状细胞 (DC) 前体从血液到外周部位的迁移，并控制成熟 DC 从炎症部位到淋巴结的迁移。因此，Cd38(-/-)小鼠中T细胞的启动效率低下，导致体液免疫反应较差。我们还表明，CD38 和 cADPR 调节趋化因子刺激的 DC 中的钙动员，并且是未成熟和成熟 DC 对 CCL2、CCL19、CCL21 和 CXCL12 的趋化性所必需的。因此，CD38 通过控制 DC 中的趋化因子受体信号传导来调节适应性免疫。
Mice lacking CD38, an ectoenzyme that generates the calcium-mobilizing metabolite cADPR, make reduced T cell-dependent antibody responses. Despite the predicted role for CD38 in B cell activation, we find that CD38 regulates the migration of dendritic cell (DC) precursors from the blood to peripheral sites and controls the migration of mature DCs from sites of inflammation to lymph nodes. Thus, T cells are inefficiently primed in Cd38(-/-) mice, leading to poor humoral immune responses. We also show that CD38 and cADPR modulate calcium mobilization in chemokine-stimulated DCs and are required for the chemotaxis of immature and mature DCs to CCL2, CCL19, CCL21, and CXCL12. Therefore, CD38 regulates adaptive immunity by controlling chemokine receptor signaling in DCs.