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Updated: Jan 30, 2026

Real-Time Proxy-Control of Re-Parameterized Peripheral Signals using a Close-Loop Interface
Published on: May 8, 2021
Dock5 controls the peripheral B cell differentiation via regulating BCR signaling and actin reorganization
Anwei Chen1, Di Yang2, Xingtian Xuan3
1Chongqing Key Laboratory of Child Infection and Immunity, Children's Hospital of Chongqing Medical University, Chongqing, China; Department of Pediatric Research Institute, Children's Hospital of Chongqing Medical University, Chongqing, China; Ministry of Education Key Laboratory of Child Development and Disorders, Children's Hospital of Chongqing Medical University, Chongqing, China; China International Science and Technology Cooperation Base of Child Development and Critical Disorders, China; Department of Dermatology, Children's Hospital of Chongqing Medical University, Chongqing, China.
Abstract:
As an atypical guanine nucleotide exchange factor (GEF), Dock5 has been extensively studied in cellular functions. However, the role of Dock5 on B-cell immunity still remain elusive. In this study, we generated a Dock5 knockout mouse model to study the effect of Dock5 deficiency on B cell development, differentiation and BCR signaling. We found that the absence of Dock5 leads to a moderate effect on B cell development in the bone marrow and reduces follicular (FO) and marginal zone (MZ) B cells. Mechanistically, the key positive upstream B-cell receptor (BCR) signaling molecules, CD19 and Brutons tyrosine kinase (Btk), whose activation determines the fate of FO and MZ B cells, is reduced in Dock5 KO B cells upon antigenic stimulation by using total internal reflection fluorscence microscopy (TIRF) and immunoblot. Interestingly we found that the cellular filamentous actin (F-actin), also decreased in Dock5 KO B cells upon stimulation, which, in turn, offers feedback to BCR signaling. Our study has unveiled that Dock5 regulates the peripheral B cell differentiation via controlling the CD19-Btk signaling axis as well as actin reorganization.
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