B cell receptor-induced Ca2+ mobilization mediates F-actin rearrangements and is indispensable for adhesion and spreading of B lymphocytes

Journal of Leukocyte Biology

Nóra SzilÃgyi¹  MÃté Maus⁴  David Medgyesi²  JÃnos Matkó and⁴  Gabriella SÃrmay⁴  Endre Kiss⁴  Andrea E. Schneider⁴  Ágnes Enyedi³ 

[1] Physiology and Neurobiology, Eötvös LórÃnd University, Budapest, Hungary; Department of Molecular Immunology, Max Planck Institute of Immunology, Freiburg, Germany;Department of Molecular Cell Biology, National Blood Center, Budapest, Hungary Physiology and Neurobiology, Eötvös LórÃnd University, Budapest, Hungary;Departments of Immunology and Physiology and Neurobiology, Eötvös LórÃnd University, Budapest, Hungary;

关键词: B cell spreading;    membrane-bound antigens;    B cell activation;    Ca²⁺ signal;    cofilin;   

DOI  :  10.1189/jlb.0312169

学科分类：生理学

来源: Federation of American Societies for Experimental Biology

【 摘 要 】

B cells acquire membrane-bound cognate antigens from the surface of the APCs by forming an IS, similar to that seen in T cells. Recognition of membrane-bound antigens on the APCs initiates adhesion of B lymphocytes to the antigen-tethered surface, which is followed by the formation of radial lamellipodia-like structures, a process known as B cell spreading. The spreading response requires the rearrangement of the submembrane actin cytoskeleton and is regulated mainly via signals transmitted by the BCR. Here, we show that cytoplasmic calcium is a regulator of actin cytoskeleton dynamics in B lymphocytes. We find that BCR-induced calcium mobilization is indispensible for adhesion and spreading of B cells and that PLCγ and CRAC-mediated calcium mobilization are critical regulators of these processes. Measuring calcium and actin dynamics in live cells, we found that a generation of actin-based membrane protrusion is strongly linked to the dynamics of a cytoplasmic-free calcium level. Finally, we demonstrate that PLCγ and CRAC channels regulate the activity of actin-severing protein cofilin, linking BCR-induced calcium signaling to the actin dynamics.

【 授权许可】

Unknown