Chloride ion plays critical roles in modulating immunological interactions. Herein, we demonstrated that the anion channel CLIC2α mediates Cl⁻ flux to regulate hemocytes functions in the Pacific oyster (Crassostrea gigas). Specifically, during infection by Vibrio parahemolyticus, chloride influx was activated following onset of phagocytosis. Phosphorylation of Akt was stimulated by Cl⁻ ions entering host cells, further contributing to signal transduction regulating internalization of bacteria through the PI3K/Akt signaling pathway. Concomitantly, Cl⁻ entered phagosomes, promoted the acidification and maturation of phagosomes, and contributed to production of HOCl to eradicate engulfed bacteria. Finally, genomic screening reveals CLIC2α as a major Cl⁻ channel gene responsible for regulating Cl⁻ influx in oysters. Knockdown of CLIC2α predictably impeded phagosome acidification and restricted bacterial killing in oysters. In conclusion, our work has established CLIC2α as a prominent regulator of Cl⁻ influx and thus Cl⁻ function in C. gigas in bacterial infection contexts.

氯离子在调节免疫相互作用中起关键作用。在本文中，我们表明，该阴离子通道CLIC2α介导氯^-通量调节在太平洋牡蛎（血细胞功能牡蛎）。具体而言，在副溶血性弧菌感染期间，吞噬作用开始后，氯离子流入被激活。Akt磷酸化被刺激经Cl ^-离子进入宿主细胞中，通过PI3K / Akt信号传导途径进一步促进细菌的信号转导调节内化。与此同时，氯^-进入吞噬体，促进吞噬体的酸化和成熟，并促进了HOCl的产生以根除被吞噬的细菌。最后，基因组筛选揭示CLIC2α作为主要氯^-负责调节氯通道基因^-牡蛎涌入。剔除CLIC2α可以预期阻止牡蛎的吞噬体酸化并限制细菌的杀死。总之，我们的工作已经建立CLIC2α为氯的一个突出的调节^-涌入，从而氯^-功能C.牡蛎中的细菌感染的上下文。