Clinical and Translational Allergy (Feb 2022)

IgE and high‐affinity IgE receptor in chronic inducible urticaria, pathogenic, and management relevance

  • Ana M. Giménez‐Arnau,
  • Clara Ribas‐Llauradó,
  • Nasser Mohammad‐Porras,
  • Gustavo Deza,
  • Ramón M. Pujol,
  • Ramón Gimeno

DOI
https://doi.org/10.1002/clt2.12117
Journal volume & issue
Vol. 12, no. 2
pp. n/a – n/a

Abstract

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Abstract Background IgE and high‐affinity IgE receptor (FcεRI) expression on basophils have been scarcely explored in patients with chronic inducible urticaria (CIndU). Objectives To investigate baseline serum IgE and FcεRI expression on blood basophils in a large cohort of CIndU patients and its relationship to treatment response. Methods Baseline total serum IgE and basophil FcεRI expression measured by flow cytometry in 165 patients with CIndU was studied. The relationship of both parameters with the response to antihistamine and anti‐IgE (omalizumab) treatment was considered in a subsample of CIndU patients. FcεRI expression in basophils was assessed by mean fluorescence intensity (MFI) and basophil FcεRI standardized density (receptors/cell). Results The median FcεRI expression standardized per density in blood basophils was found significantly higher in patients with CIndU compared to HCs. A positive correlation was found between IgE serum levels and basophil FcεRI expression. Basal FcεRI expression was not related to antihistamine treatment response. However, it was related to omalizumab, and patients responding to omalizumab showed higher basal basophil expression of FcεRI levels. Non‐responders to the antihistamine showed significantly higher IgE serum levels. Conclusions FcεRI receptor overexpression in patients with CIndU shows almost the same pattern than chronic spontaneous urticaria. It seems to be independent of CIndU subtypes. Although additional studies would be welcome, our work highlights the relevance of FcεRI receptor regulation in CIndU supporting autoimmune basophil and mast cell activation and may be a biomarker for response to anti‐IgE therapy.

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