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

Máté Maus, David Medgyesi, Endre Kiss, Andrea E. Schneider, Ágnes Enyedi, Nóra Szilágyi, János Matkó, Gabriella Sármay

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17 Citations (Scopus)


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.

Original languageEnglish
Pages (from-to)537-547
Number of pages11
JournalJournal of Leukocyte Biology
Issue number4
Publication statusPublished - Apr 1 2013



  • B cell activation
  • B cell spreading
  • Ca
  • Cofilin
  • Membrane-bound antigens
  • Signal

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Cell Biology

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