Ion channel TRPV2 is critical in enhancing B cell activation and function
Cuifeng Li, Meng Zhao, Xiaohang Liu, Yuxin Li, Bihua Xu, L. Zhou, Xiaolin Sun, Wenbo Sun, Na Kang, Zhenglin Ji, Tong Li, Haoran An, Fei Wang, Chuan Wu, Jingying Ye, Jing‐Ren Zhang, Qingwen Wang, Xiaodong Zhao, Zhanguo Li, Wanli Liu
Abstract
The function of transient receptor potential vanilloid (TRPV) cation channels governing B cell activation remains to be explored. We present evidence that TRPV2 is highly expressed in B cells and plays a crucial role in the formation of the B cell immunological synapse and B cell activation. Physiologically, TRPV2 expression level is positively correlated to influenza-specific antibody production and is low in newborns and seniors. Pathologically, a positive correlation is established between TRPV2 expression and the clinical manifestations of systemic lupus erythematosus (SLE) in adult and child SLE patients. Correspondingly, mice with deficient TRPV2 in B cells display impaired antibody responses following immunization. Mechanistically, the pore and N-terminal domains of TRPV2 are crucial for gating cation permeation and executing mechanosensation in B cells upon antigen stimulation. These processes synergistically contribute to membrane potential depolarization and cytoskeleton remodeling within the B cell immunological synapse, fostering efficient B cell activation. Thus, TRPV2 is critical in augmenting B cell activation and function.