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 Blood, 1 December 2007, Vol. 110, No. 12, pp. 3985-3995.
Prepublished online as a Blood First Edition Paper on August 27, 2007; DOI 10.1182/blood-2007-05-088468.

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IMMUNOBIOLOGY

Extracellular calcium sensing promotes human B-cell activation and function

Caitlin M. Hammond1,2, Dionne White1, Jelena Tomic1,2, Yonghong Shi1, and David E. Spaner1,3

1 Division of Molecular and Cellular Biology, Sunnybrook Research Institute, Sunnybrook Health Sciences Centre, Toronto, ON; 2 Department of Medical Biophysics, University of Toronto, Toronto, ON; and 3 Toronto-Sunnybrook Regional Cancer Centre, Toronto, ON

Calcium is a second messenger for many signaling pathways in B cells, but its role as a receptor ligand has not been well characterized. However, pulses of free calcium were found to cause the rapid release of internal calcium stores in normal human B cells. This response appeared to be mediated by a cell surface protein with receptor properties as it could be blocked by pretreatment with trypsin and with kinase and phospholipase C{gamma} inhibitors. The calcium receptor on B cells was not the conventional calcium-sensing receptor (CaSR) since B cells did not express CaSR and calcium-induced responses could not be blocked by specific CaSR inhibitors. B-cell responses to extracellular calcium activated phosphoinositide-3 kinase/AKT, calcineurin, extracellular signal regulated kinase, p38 mitogen-activated protein kinase, protein kinase C, Ca2+/calmodulin kinase II, and nuclear factor-{kappa}B signaling pathways, and resulted in transcription of the early response gene, CD83. This extracellular calcium sensor enhanced B-cell responses to Toll-like receptor, B-cell receptor, and cytokine receptor agonists. These findings suggest a means by which B cells prepare to engage in immune responses by responding to calcium fluctuations in their environment.


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