Mice deficient in sphingosine 1-phosphate receptor type 2 (S1P(2)) develop diffuse large B cell lymphoma. However, the role of S1P(2) in normal germinal center (GC) physiology is unknown. Here we show that S1P(2)-deficient GC B cells outgrew their wild-type counterparts in chronically established GCs. We found that antagonism of the kinase Akt mediated by S1P(2) and its downstream mediators Gα(12), Gα(13) and p115RhoGEF regulated cell viability and was required for growth control in chronically proliferating GCs. Moreover, S1P(2) inhibited GC B cell responses to follicular chemoattractants and helped confine cells to the GC. In addition, S1P(2) overexpression promoted the centering of activated B cells in the follicle. We suggest that by inhibiting Akt activation and migration, S1P(2) helps restrict GC B cell survival and localization to an S1P-low niche at the follicle center.
Pubmed ID: 21642988 RIS Download
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View all literature mentionslaboratory mouse with name STOCK Tg(ACTA1-cre)79Jme/J from MGI.
View all literature mentionsMus musculus with name B6.SJL-Ptprca Pepc/BoyJ from IMSR.
View all literature mentionsCell line Ramos is a Cancer cell line with a species of origin Homo sapiens (Human)
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