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.
journal_name
Cell Immunoljournal_title
Cellular immunologyauthors
Chen A,Yang D,Xuan X,Miller H,Luo X,Yu J,Yang G,Wang H,Liu Cdoi
10.1016/j.cellimm.2019.01.001subject
Has Abstractpub_date
2019-03-01 00:00:00pages
15-21eissn
0008-8749issn
1090-2163pii
S0008-8749(18)30465-9journal_volume
337pub_type
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journal_title:Cellular immunology
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journal_title:Cellular immunology
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journal_title:Cellular immunology
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