EBI2 regulates CXCL13-mediated responses by heterodimerization with CXCR5
EBI2 regulates CXCL13-mediated responses by heterodimerization with CXCR5
复制标题
DOI：
10.1096/fj.12-208876
复制
发表时间：
2012-12-01
期刊：
影响因子：
4.8
通讯作者：
Mellado, Mario
中科院分区：
文献类型：
--
作者：
Barroso, Ruben;Martinez Munoz, Laura;Mellado, Mario
B细胞进入淋巴滤泡的运动取决于趋化因子受体CXCR 5和最近报道的EB病毒诱导受体2（EBI 2）的表达。EBI 2与CXCR 5合作，帮助将激活的B细胞定位在卵泡中，尽管其机制尚不清楚。使用人HEK 293 T细胞和荧光共振能量转移（FRET）技术，我们证明CXCR 5和EBI 2形成同源和异源二聚体。EBI 2表达调节CXCR 5同源二聚体复合物，如FRET 50值所示（CXCR 5同源二聚体，0.9851 +/- 0.0784; CXCR 5同源二聚体+EBI 2，1.7320 +/- 0.4905; P
B-cell movement into lymphoid follicles depends on the expression of the chemokine receptor CXCR5 and the recently reported Epstein-Barr virus-induced receptor 2 (EBI2). In cooperation with CXCR5, EBI2 helps to position activated B cells in the follicle, although the mechanism is poorly understood. Using human HEK293T cells and fluorescence resonance energy transfer (FRET) techniques, we demonstrate that CXCR5 and EBI2 form homo- and heterodimers. EBI2 expression modulated CXCR5 homodimeric complexes, as indicated by the FRET50 value (CXCR5 homodimer, 0.9851 +/- 0.0784; CXCR5 homodimer+EBI2, 1.7320 +/- 0.4905; P