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S Shaheen, Z Wan, Z Li, A Chau, X Li, S Zhang, Y Liu, J Yi, Y Zeng, J Wang, X Chen, L Xu, W Chen, F Wang, Y Lu, W Zheng, Y Shi, X Sun, Z Li, C Xiong and W Liu
Abstract
The mechanosensing ability of lymphocytes regulates their activation in response to antigen stimulation, but the underlying mechanism remains unexplored. Here, we report that B cell mechanosensing-governed activation requires BCR signaling molecules. PMA-induced activation of PKCβ can bypass the Btk and PLC-γ2 signaling molecules that are usually required for B cells to discriminate substrate stiffness. Instead, PKCβ-dependent activation of FAK is required, leading to FAK-mediated potentiation of B cell spreading and adhesion responses. FAK inactivation or deficiency impaired B cell discrimination of substrate stiffness. Conversely, adhesion molecules greatly enhanced this capability of B cells. Lastly, B cells derived from rheumatoid arthritis (RA) patients exhibited an altered BCR response to substrate stiffness in comparison with healthy controls. These results provide a molecular explanation of how initiation of B cell activation discriminates substrate stiffness through a PKCβ-mediated FAK activation dependent manner.
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Concepts
T cell, Lymphocyte, B cell, Discrimination, Focal adhesion, Enzyme, Rheumatoid arthritis, Protein
MeSH headings
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