The calcium-activated nonselective cation channel TRPM4 is essential for the migration but not the maturation of dendritic cells.
The calcium-activated nonselective cation channel TRPM4 is essential for the migration but not the maturation of dendritic cells.
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树突状细胞（DC）的成熟和迁移是免疫应答启动的关键事件。在遇到病原体后，DC上调共刺激分子的表达，随后迁移到次级淋巴器官。钙离子（Ca2+）进入控制许多造血细胞类型的功能，但Ca2+进入在DC生物学中的作用仍不清楚。在这里，我们报告，钙激活的非选择性阳离子通道TRPM4的表达和控制小鼠DC的钙稳态。TRPM4的缺乏，引起Ca2+超载，不影响DC成熟，但大大损害趋化因子依赖性DC迁移。我们的研究结果建立了TRPM4调节的Ca2+稳态对DC的流动性至关重要，但不是成熟，并强调DC的成熟和迁移是独立调节的。
Dendritic cell (DC) maturation and migration are events critical for the initiation of immune responses. After encountering pathogens, DCs upregulate the expression of costimulatory molecules and subsequently migrate to secondary lymphoid organs. Calcium (Ca2+) entry governs the functions of many hematopoietic cell types, but the role of Ca2+ entry in DC biology remains unclear. Here we report that the Ca2+-activated nonselective cation channel TRPM4 was expressed in and controlled the Ca2+ homeostasis of mouse DCs. The absence of TRPM4, which elicited Ca2+ overload, did not influence DC maturation but did considerably impair chemokine-dependent DC migration. Our results establish TRPM4-regulated Ca2+ homeostasis as crucial for DC mobility but not maturation and emphasize that DC maturation and migration are independently regulated.