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Updated: Apr 4, 2026
Flow Cytometric Characterization of Murine B Cell Development
Published on: January 22, 2021
Kidins220/ARMS binds to the B cell antigen receptor and regulates B cell development and activation
Gina J Fiala1, Iga Janowska2, Fabiola Prutek2
1Department of Molecular Immunology, BioIII, Faculty of Biology, University of Freiburg and Max Planck Institute of Immunobiology and Epigenetics, 79104 Freiburg, Germany Centre for Biological Signaling Studies (BIOSS), Spemann Graduate School of Biology and Medicine (SGBM), Centre of Chronic Immunodeficiency (CCI), Department of Dermatology, Center for Biological Systems Analysis (ZBSA), Institute of Molecular Medicine and Cell Research, Comprehensive Cancer Centre Freiburg, and Institute of Pathology, University Medical Center Freiburg, University of Freiburg, 79104 Freiburg, Germany Centre for Biological Signaling Studies (BIOSS), Spemann Graduate School of Biology and Medicine (SGBM), Centre of Chronic Immunodeficiency (CCI), Department of Dermatology, Center for Biological Systems Analysis (ZBSA), Institute of Molecular Medicine and Cell Research, Comprehensive Cancer Centre Freiburg, and Institute of Pathology, University Medical Center Freiburg, University of Freiburg, 79104 Freiburg, Germany Centre for Biological Signaling Studies (BIOSS), Spemann Graduate School of Biology and Medicine (SGBM), Centre of Chronic Immunodeficiency (CCI), Department of Dermatology, Center for Biological Systems Analysis (ZBSA), Institute of Molecular Medicine and Cell Research, Comprehensive Cancer Centre Freiburg, and Institute of Pathology, University Medical Center Freiburg, University of Freiburg, 79104 Freiburg, Germany.
Abstract:
B cell antigen receptor (BCR) signaling is critical for B cell development and activation. Using mass spectrometry, we identified a protein kinase D-interacting substrate of 220 kD (Kidins220)/ankyrin repeat-rich membrane-spanning protein (ARMS) as a novel interaction partner of resting and stimulated BCR. Upon BCR stimulation, the interaction increases in a Src kinase-independent manner. By knocking down Kidins220 in a B cell line and generating a conditional B cell-specific Kidins220 knockout (B-KO) mouse strain, we show that Kidins220 couples the BCR to PLCγ2, Ca(2+), and extracellular signal-regulated kinase (Erk) signaling. Consequently, BCR-mediated B cell activation was reduced in vitro and in vivo upon Kidins220 deletion. Furthermore, B cell development was impaired at stages where pre-BCR or BCR signaling is required. Most strikingly, λ light chain-positive B cells were reduced sixfold in the B-KO mice, genetically placing Kidins220 in the PLCγ2 pathway. Thus, our data indicate that Kidins220 positively regulates pre-BCR and BCR functioning.
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