Mast cells induce the inflammatory process when their FcepsilonRI receptors aggregate in response to an antigen binding to immunoglobulin E. Direct interactions between FcepsilonRI receptor cytoplasmic domains and various intracellular proteins initiate diverse signal transduction pathways resulting in the immediate release of proinflammatory agents. A delayed response also occurs that includes the release of various cytokines. It is clear that the activation of kinases, such as protein kinase C (PKC), is a requirement for both the early and delayed responses of this inflammatory process. In this review we present the results of various studies investigating the role of PKC isozymes in mast cells.
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Nechushtan et al. (2001) studied this question.
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