A redundant role for PKC-ε in mast cell signaling and effector function

Lessmann, Eva; Leitges, Michael; Huber, Michael

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A redundant role for PKC-ε in mast cell signaling and effector function

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Lessmann, Eva
Research Group and Chair of Molecular Immunology of the University of Freiburg, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Huber, Michael
Research Group and Chair of Molecular Immunology of the University of Freiburg, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Lessmann, E., Leitges, M., & Huber, M. (2006). A redundant role for PKC-ε in mast cell signaling and effector function. International Immunology, 18, 767-773.

Cite as: https://hdl.handle.net/11858/00-001M-0000-002B-9292-D

Abstract

Protein kinase (PK) C-ε is strongly expressed in mast cells (MCs) and activated in response to antigen-mediated high-affinity receptor for IgE (FcεR1) engagement. A critical role of PKC-ε in antigen-triggered activation of various signaling pathways was observed in basophilic leukemia cells. To study the function of PKC-ε in MCs differentiated in vitro from murine bone marrow, we used our established PKC-ε null mice. Unexpectedly, we did not reveal any difference in antigen-induced activation of many central signaling molecules (PKB, mitogen-activated protein kinase, p38, Jun-N-terminal kinase, phospholipase C-γ1, Bruton's tyrosine kinase, PKD, Fos and PKC-δ) in time-course as well as dose-response studies between PKC-ε-deficient and wild-type MCs. In correlation, antigen-triggered degranulation, release of arachidonic acid and secretion of IL-6 were unaltered by the loss of PKC-ε. Furthermore, stimulation of MCs via different receptor systems [Steel factor receptor (c-kit) and toll-like receptor 4] did not lead to differences in the measured responses between both cell types. These results strongly suggest that PKC-ε plays a redundant role in MCs stimulated by antigen as well as other well-known MC stimuli.