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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. This Article Full Text (PDF) All Versions of this Article: blood-2007-05-088468v1 110/12/3985    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Hammond, C. M Articles by Spaner, D. E Search for Related Content PubMed PubMed Citation Articles by Hammond, C. M Articles by Spaner, D. E Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted May 2, 2007 Accepted August 22, 2007 Extracellular calcium sensing promotes human B cell activation and function Caitlin M Hammond, Dionne White, Jelena Tomic, Yonghong Shi, and David E Spaner* Division of Molecular and Cellular Biology, Sunnybrook Research Institute, Sunnybrook Health Sciences Centre, Toronto, Ontario, Canada Department of Medical Biophysics, University of Toronto, Toronto, Ontario, Canada Toronto-Sunnybrook Regional Cancer Centre, Toronto, Ontario, Canada * Corresponding author; email: david.spaner{at}swri.ca. 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 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-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. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: T. Lyubchenko, J. P. Nielsen, S. M. Miller, G. A. Liubchenko, and V. M. Holers Role of initial protein phosphorylation events and localized release-activated calcium influx in B cell antigen receptor signaling J. Leukoc. Biol., February 1, 2009; 85(2): 298 - 309. [Abstract] [Full Text] [PDF]

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