Mice deficient in sphingosine 1-phosphate receptor type 2 (S1P₂) develop diffuse large B cell lymphoma. However, the role of S1P₂ in normal germinal center (GC) physiology is unknown. Here we show that S1P₂-deficient GC B cells outgrew their wild-type counterparts in chronically established GCs. We found that antagonism of the kinase Akt mediated by S1P₂ and its downstream mediators Gα₁₂, Gα₁₃ and p115RhoGEF regulated cell viability and was required for growth control in chronically proliferating GCs. Moreover, S1P₂ inhibited GC B cell responses to follicular chemoattractants and helped confine cells to the GC. In addition, S1P₂ overexpression promoted the centering of activated B cells in the follicle. We suggest that by inhibiting Akt activation and migration, S1P₂ helps restrict GC B cell survival and localization to an S1P-low niche at the follicle center.