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Background  Chloroquine, a bitter tastant, inhibits Ca 2+  signaling, resulting in suppression of B cell activation; however, the inhibitory mechanism remains unclear.    Results  In this study, thapsigargin (TG), but not caffeine, induced sustained intracellular Ca 2+  increases in mouse splenic primary B lymphocytes, which were markedly inhibited by chloroquine. Under Ca 2+ -free conditions, TG elicited transient Ca 2+  increases, which additionally elevated upon the restoration of 2 mM Ca 2+ . The former were from release of intracellular Ca 2+  store and the latter from Ca 2+  influx. TG-induced release was inhibited by 2-APB (an inhibitor of inositol-3-phosphate receptors, IP 3 Rs) and chloroquine, and TG-caused influx was inhibited by pyrazole (Pyr3, an inhibitor of transient receptor potential C3 (TRPC3) and stromal interaction molecule (STIM)/Orai channels) and chloroquine. Moreover, chloroquine also blocked Ca 2+  increases induced by the engagement of B cell receptor (BCR) with anti-IgM.    Conclusions  These results indicate that chloroquine inhibits Ca 2+  elevations in splenic B cells through inhibiting Ca 2+  permeable IP 3 R and TRPC3 and/or STIM/Orai channels. These findings suggest that chloroquine would be a potent immunosuppressant.

Chloroquine inhibits Ca2+ permeable ion channels-mediated Ca2+ signaling in primary B lymphocytes