Abstract

Immunoglobulin E (IgE) is a well-known key factor in allergic airway disease; however, its central role in non-allergic airway inflammation is often underestimated. In some airway diseases, IgE is produced as a result of allergic sensitization. However, in others, IgE production occurs despite the lack of a specific allergen. Although multiple pathways contribute to the production of IgE in airway disease, it is its activity in mediating the inflammatory response that is associated with disease. Therefore, an understanding of IgE as the unifying component of upper and lower airway diseases has important implications for both diagnosis and treatment. Understanding the role of IgE in each upper and lower airway disease highlights its potential utility as a diagnostic marker and therapeutic target. Further classification of these diseases by whether they are IgE mediated or non–IgE mediated, rather than by the existence of an underlying allergic component, accounts for both systemic and localized IgE activity. Improvements in diagnostic methodologies and standardization of clinical practices with this classification in mind can help identify patients with IgE-mediated diseases. In doing so, this group of patients can receive optimal care through targeted anti-IgE therapeutics, which have already demonstrated efficacy across numerous IgE-mediated upper and lower airway diseases.

Highlights

  • Immunoglobulin E (IgE) is widely accepted as an integral component of the pathogenesis of many allergic respiratory diseases, with increasing recognition of involvement in the non-allergic forms of disease. This is evident in both upper airway diseases, including allergic rhinitis (AR), non-allergic rhinitis (NAR), and chronic rhinosinusitis with nasal polyps (CRSwNP), and lower airway diseases, including allergic asthma and non-allergic asthma phenotypes [1]

  • IgE is routinely described in the pathology of both acute and chronic inflammatory allergic diseases [11], and elevated IgE levels are commonly reported in non-allergic late-onset asthma and nasal polyps (NP), in which the emergence of

  • There is considerable evidence supporting the role of IgE in many upper and lower airway diseases as the underlying cause of damaging inflammation independent of allergy [1, 33]

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Summary

Introduction

Immunoglobulin E (IgE) is widely accepted as an integral component of the pathogenesis of many allergic respiratory diseases, with increasing recognition of involvement in the non-allergic forms of disease. The polyclonal IgE produced following S. aureus superantigen exposure can contribute to the persistent type 2 inflammation associated with CRSwNP through continuous mast cell activation, and the elevated specific polyclonal IgE to S. aureus enterotoxins in the serum of these patients is a known risk factor for asthma severity [23].

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