Leupaxin Expression Is Dispensable for B Cell Immune Responses.

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Bonaud, Amélie 
Clare, Simon 
Bisio, Valeria 
Sowerby, John M 
Yao, Shugang 

The generation of a potent humoral immune response by B cells relies on the integration of signals induced by the B cell receptor, toll-like receptors and both negative and positive co-receptors. Several reports also suggest that integrin signaling plays an important role in this process. How integrin signaling is regulated in B cells is however still partially understood. Integrin activity and function are controlled by several mechanisms including regulation by molecular adaptors of the paxillin family. In B cells, Leupaxin (Lpxn) is the most expressed member of the family and in vitro studies suggest that it could dampen BCR signaling. Here, we report that Lpxn expression is increased in germinal center B cells compared to naïve B cells. Moreover, Lpxn deficiency leads to decreased B cell differentiation into plasma cells in vitro. However, Lpxn seems dispensable for the generation of a potent B cell immune response in vivo. Altogether our results suggest that Lpxn is dispensable for T-dependent and T-independent B cell immune responses.

B cells, cell activation, humoral immune response, leupaxin, plasma cells, Animals, Antibody Formation, B-Lymphocytes, Cell Adhesion Molecules, Cell Differentiation, Cells, Cultured, Germinal Center, Immunity, Humoral, Lymphocyte Activation, Mice, Mice, Knockout, Plasma Cells, Receptors, Antigen, B-Cell, Signal Transduction, Transcription Factors
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Front Immunol
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Frontiers Media SA
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Wellcome Trust (083650/Z/07/Z)
This work was funded by a Junior Team Leader starting grant from the Laboratory of Excellence in Research on Medication and Innovative Therapeutics (LabEx LERMIT) supported by a grant from ANR (ANR-10-LABX-33 to ME) under the program “Investissements d'Avenir” (ANR-11-IDEX-0003-01) and by an ANR @RAction starting grant (ANR-14-ACHN-0008 to ME) and by the Wellcome-Trust (Programme Grant Number 083650/Z/07/Z to KGCS) and VB is supported by INCa grant (PRT-K 2017).