IgE enhances FcεRI expression and IgE-dependent TNF-α release from canine skin mast cells

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Abstract

The role of IgE on mast cell (MC) activation is well known. Recent studies have demonstrated that IgE also has the ability to up-regulate the high affinity IgE receptor (FcεRI) on the surface of human and murine MC, leading to an increased production of cytokines and chemokines. In the present study, we have examined the influence of IgE levels on FcεRI expression, and its consequences on TNF-α production from canine skin MC. Mature MC were enzymatically dispersed from the skin biopsies of 6-8 dogs and were cultured for up to 5 days in medium supplemented with recombinant canine stem cell factor (SCF) (6ng/ml), in the presence of increasing serum IgE concentrations (ranging from 0 to 80μg/ml). Subsequently, skin MC were activated with anti-IgE, and TNF-α concentration was assessed 5h post-activation by a cytotoxic bioassay. FcεRI receptors were identified in MC surface by flow cytometry. MC cultured for up to 5 days in the presence of high serum IgE concentration (8μg/ml) produced twice the quantity of TNF-α than MC cultured in the absence of serum IgE, in response to stimulation with anti-IgE. Moreover, the percentage of FcεRI-positive skin cells was found to be approximately double in cells cultured with serum IgE compared to that cultured in the absence of IgE, following saturation of IgE receptors. These results suggest that, as found in human and murine MC, IgE may induce an up-regulation of the FcεRI density and an enhancement in the secretory activity of canine skin MC. This study could be of great interest in designing new therapeutic strategies for controlling MC activation in inflammatory and allergic processes. © 2002 Elsevier Science B.V. All rights reserved.
Original languageEnglish
Pages (from-to)205-212
JournalVeterinary Immunology and Immunopathology
Volume85
Issue number3-4
DOIs
Publication statusPublished - 15 Apr 2002

Keywords

  • Canine mast cell
  • High affinity IgE receptor
  • IgE
  • TNF-α

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