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Activation of mast cells by immunoglobulin E-receptor cross-linkage, but not through adenosine receptors, induces A1 expression and promotes survival


Dr Gunnar Nilsson, The Rudbeck Laboratory, Department of Genetics and Pathology, Uppsala University, SE-751 85 Uppsala, Sweden. E-mail:


Background Mast cells are a potent source of mediators that regulate the inflammatory response in allergy and asthma. Mast cells can be activated through different receptors, for example, via cross-linkage of the high-affinity IgE receptor (FcɛRI) and by adenosine acting on specific receptors. We have recently described mast cell survival of an IgE receptor activation by up-regulation of the anti-apoptotic gene A1.

Objective To compare mast cell survival and expression of A1 after activation through the FcɛRI and by an adenosine agonist.

Methods Bone marrow-derived, cultured mouse mast cells (BMCMC) were activated either with IgE+antigen or with the adenosine receptor agonist 5′-N-ethylcarboxamido adenosine (NECA). Release of β-hexosaminidase, cell viability, phosphorylation of Akt and IkB-α, and expression of pro-survival and pro-apoptotic genes were measured after activation.

Results Activation of BMCMC with NECA caused the release of β-hexosaminidase, although to a lesser extent than after FcɛRI activation (33% and 98%, respectively). Activation by both NECA and FcɛRI stimulated phosphorylation of Akt (Ser473 and Thr308) and IkB-α (Ser32), both of which are implicated in the regulation of cell survival. However, only cells that were activated through FcɛRI, but not by NECA, expressed A1 and exhibited an increased survival rate compared to the control.

Conclusion These results show that adenosine receptor activation of BMCMC does not induce the same survival programme in mast cells as does activation through FcɛRI. These findings may be important for understanding the role that mast cells play in asthma provoked by different stimuli.