Förster R, Mattis A E, Kremmer E, Wolf E, Brem G, Lipp M
Max-Delbrück-Center for Molecular Medicine, Berlin-Buch, Germany.
Cell. 1996 Dec 13;87(6):1037-47. doi: 10.1016/s0092-8674(00)81798-5.
We describe the phenotype of gene-targeted mice lacking the putative chemokine receptor BLR1. In normal mice, this receptor is expressed on mature B cells and a subpopulation of T helper cells. Blr1 mutant mice lack inguinal lymph nodes and possess no or only a few phenotypically abnormal Peyer's patches. The migration of lymphocytes into splenic follicles is severely impaired, resulting in morphologically altered primary lymphoid follicles. Furthermore, activated B cells fail to migrate from the T cell-rich zone into B cell follicles of the spleen, and despite high numbers of germinal center founder cells, no functional germinal centers develop in this organ. Our results identify the putative chemokine receptor BLR1 as the first G protein-coupled receptor involved in B cell migration and localization of these cells within specific anatomic compartments.
我们描述了缺乏假定趋化因子受体BLR1的基因靶向小鼠的表型。在正常小鼠中，该受体在成熟B细胞和辅助性T细胞亚群上表达。Blr1突变小鼠缺乏腹股沟淋巴结，且没有或仅有少数表型异常的派尔集合淋巴结。淋巴细胞向脾滤泡的迁移严重受损，导致初级淋巴滤泡形态改变。此外，活化的B细胞无法从富含T细胞的区域迁移至脾脏的B细胞滤泡，并且尽管生发中心起始细胞数量众多，但该器官中并未形成功能性生发中心。我们的结果确定了假定趋化因子受体BLR1是首个参与B细胞迁移以及这些细胞在特定解剖区域定位的G蛋白偶联受体。
