Lysophospholipids (LPLs) such as lysophosphatidic acid (LPA) and sphingosine 1-phosphate (S1P) are chemotactic for lymphocytes, and increases of in cytosolic [$Ca^{2+}$] signal the regulation of lymphocyte activation and migration. Here, the authors investigated the effects of LPA and S1P on $[Ca^{2+}]_c$ in mouse B cell lines (WEHI-231 and Bal-17) and primary B cells isolated from mouse spleen and bone marrow, and focused on the modulation of store-operated $Ca^{2+}$ entry (SOCE) by LPLs. In Bal-17 (a mature B cell line) both LPA and S1P induced a transient $[Ca^{2+}]_c$ increase via a phospholipase C pathway. In addition, pretreatment with LPLs was found to augment thapsigargin-induced SOCE in Bal-17 cells. However, in WEHI-231 (an immature B cell line) LPLs had no significant effect on $[Ca^{2+}]_c$ or SOCE. Furthermore, in freshly isolated splenic B cells (SBCs) and bone marrow B cells (BMBCs), LPLs induced only a small increase in $[Ca^{2+}]_c$. Interestingly, however, pretreatment with LPLs markedly increased SOCE in primary B cells, and this augmentation was more prominent in BMBCs than SBCs. The unidirectional influx of $Ca^{2+}$ was measured using $Ba^{2+}$ as a surrogate ion. Similarly, $Ba^{2+}$ influx was also found to be markedly increased by LPLs in SBCs and BMBCs. Summarizing, LPLs were found to strongly augment SOCE-mediated $Ca^{2+}$-signaling in mouse B cells. However, unlike the mature Bal-17 cell line, PLC-dependent $Ca^{2+}$ release was insignificant in primary B cells and inWEHI-231.