The calcium-activated nonselective cation channel TRPM4 is essential for the migration but not the maturation of dendritic cells

被引:170
作者
Barbet, Gaetan [1 ,2 ,3 ]
Demion, Marie [1 ,2 ,3 ]
Moura, Ivan C. [1 ,3 ]
Serafini, Nicolas [1 ,2 ,3 ]
Leger, Thibaut [1 ,2 ,3 ]
Vrtovsnik, Francois [1 ,3 ,4 ]
Monteiro, Renato C. [1 ,3 ]
Guinamard, Romain [5 ]
Kinet, Jean-Pierre [6 ,7 ]
Launay, Pierre [1 ,2 ,3 ]
机构
[1] Univ Paris 07, INSERM, U699, F-75018 Paris, France
[2] Univ Paris 07, INSERM, Equipe Avenir, F-75018 Paris, France
[3] Univ Paris 07, Fac Med, F-75018 Paris, France
[4] Hop Bichat Claude Bernard, Serv Nephrol, F-75018 Paris, France
[5] Univ Caen, Lab Physiol Cellulaire, EA 3212, F-14032 Caen, France
[6] Harvard Univ, Sch Med, Boston, MA 02215 USA
[7] Beth Israel Deaconess Med Ctr, Dept Pathol, Boston, MA 02215 USA
关键词
D O I
10.1038/ni.1648
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
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.
引用
收藏
页码:1148 / 1156
页数:9
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