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Prepublished online as a Blood First Edition Paper on April 17, 2003; DOI 10.1182/blood-2002-10-3176. This Article Full Text (PDF) All Versions of this Article: 2002-10-3176v1 102/4/1405    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 Lam, V. Articles by Krystal, G. Search for Related Content PubMed PubMed Citation Articles by Lam, V. Articles by Krystal, G. Social Bookmarking                   What's this? Submitted October 21, 2002 Accepted April 7, 2003 IgE alone stimulates mast cell adhesion to fibronectin via pathways similar to those used by IgE+ antigen but distinct from those used by Steel Factor Vivian Lam, Janet Kalesnikoff, Corinna W K Lee, Valerie Hernandez-Hansen, Bridget S Wilson, Janet M Oliver, and Gerald Krystal* Terry Fox Laboratory, British Columbia Cancer Agency, Vancouver, BC, Canada Department of Pathology and Cancer Research and Treatment Center, University of New Mexico School of Medicine, Albuquerque, NM, USA * Corresponding author; email: gkrystal{at}bccancer.bc.ca. We recently demonstrated that IgE, in the absence of crosslinking agents, activates signaling pathways in normal murine bone marrow derived mast cells (BMMCs) and that this activation enhances BMMC survival, at least in part, via secretion of autocrine-acting cytokines. We report herein that IgE alone also triggers the adhesion of both BMMCs and connective tissue mast cells (CTMCs) to the connective tissue component, fibronectin (FN). This adhesion occurs to the same extent as that triggered by optimal levels of Steel Factor (SF) or IgE + antigen (IgE+Ag) and is mediated by an increased avidity of the integrin VLA-5. Moreover, this IgE-induced adhesion, which is prolonged compared to that elicited by SF or IgE+Ag, requires phosphatidylinositol 3-kinase (PI3K), phospholipase C(PLC) and extracellular calcium but not Erk or p38. Interestingly, we found, using the calcium channel blocker, 2-APB and Lyn -/- BMMCs that both IgE- and IgE+Ag-induced adhesion to FN require extracellular calcium entry whereas SF does not. Furthermore, our data suggest that FN acts synergistically with IgE to prolong intracellular phosphorylation events and enhance IgE-induced inflammatory cytokine production and BMMC survival. 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