Fig. 2 FcRL1 deficiency impairs antigen binding–induced calcium mobilization and the in vitro proliferation of primary B cells. FcRL1 deficiency impairs.

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Fig. 2 FcRL1 deficiency impairs antigen binding–induced calcium mobilization and the in vitro proliferation of primary B cells. FcRL1 deficiency impairs antigen binding–induced calcium mobilization and the in vitro proliferation of primary B cells. (A and B) Normalized Ca2+ mobilization indicated by Fluo-4–to–Fura Red ratio in primary B cells stimulated with F(ab′)2 goat anti-mouse IgM (A) and in CH27 B cells stimulated with PC10-BSA (B). The arrows indicate the time of antigen stimulation. Experiments were repeated three times, and data from a representative experiment are shown. (C to E) Representative proliferation profiles of mouse primary B cells at 72 hours after stimulation indicated by the decreased intensity of the proliferation marker carboxyfluorescein diacetate succinimidyl ester (CFSE). Mouse WT and FcRL1-KO primary B cells were stimulated via BCR ligation (C). Mouse FcRL1-deficient primary B cells expressing HA-FcRL1(WT)-mCherry or HA-FcRL1(Y281F)-mCherry were stimulated via FcRL1 ligation (D). Mouse FcRL1-deficient primary B cells expressing HA-FcRL1(WT)-mCherry were treated with imatinib or dimethyl sulfoxide (DMSO) via stimulated by FcRL1 ligation (E). Experiments were repeated three times, and data from a representative experiment are shown. Xingwang Zhao et al. Sci Adv 2019;5:eaaw0315 Copyright © 2019 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works. Distributed under a Creative Commons Attribution NonCommercial License 4.0 (CC BY-NC).