Allergy Asthma Immunol Res.  2015 Jul;7(4):321-331. 10.4168/aair.2015.7.4.321.

Local Immunoglobulin E in the Nasal Mucosa: Clinical Implications

Affiliations
  • 1Upper Airways Research Laboratory, Department of Otorhinolaryngology, Ghent University Hospital, Ghent, Belgium. Philippe.gevaert@ugent.be
  • 2Laboratory of Immunoregulation and Mucosal Immunology, Ghent University, Ghent, Belgium.
  • 3Division of ENT Diseases, Clintec, Karolinska Institutet, Stockholm, Sweden.

Abstract

Immunoglobulin E (IgE) can be highly elevated in the airway mucosa independently of IgE serum levels and atopic status. Mostly, systemic markers are assessed to investigate inflammation in airway disease for research or clinical practice. A more accurate but more cumbersome approach to determine inflammation at the target organ would be to evaluate markers locally. We review evidence for local production of IgE in allergic rhinitis (AR) and chronic rhinosinusitis with nasal polyps (CRSwNP). Diagnostic and therapeutic consequences in clinical practice are discussed. We describe that the airway mucosa has the intrinsic capability to produce IgE. Moreover, not only do IgE-positive B cells reside within the mucosa, but all tools are present locally for affinity maturation by somatic hypermutation (SHM), clonal expansion, and class switch recombination to IgE. Recognizing local IgE in the absence of systemic IgE has diagnostic and therapeutic consequences. Therefore, we emphasize the importance of local IgE in patients with a history of AR or CRSwNP.

Keyword

local IgE; allergic rhinitis; local allergic rhinitis; chronic rhinosinusitis with nasal polyps; diagnostics; treatment

MeSH Terms

B-Lymphocytes
Humans
Immunoglobulin E*
Immunoglobulins*
Inflammation
Mucous Membrane
Nasal Mucosa*
Nasal Polyps
Recombination, Genetic
Rhinitis
Immunoglobulin E
Immunoglobulins

Figure

  • Fig. 1 Pathways resulting in local IgE production in CRSwNP. In the first part, dendritic cells of the skin and mucosa process aeroallergens deposited on the mucosa, and subsequently they present antigens to T cells. T helper 2 cells release their mediators upon recognition of antigens presented by antigen-presenting cells. The Th2 cytokines IL4, IL13, and CD40L induce selective somatic recombination of immunoglobulin heavy chain regions in B cells before maturation into IgE-producing plasma cells. IL5 stimulates eosinophil growth and differentiation. Alternatively, IgE is produced by stimulating innate lymphoid cells to release IL4, IL5, and IL13.

  • Fig. 2 Local IgE levels in nasal tissue homogenates. In the population with CRSwNP and comorbid asthma, local IgE is highly elevated, as compared to controls, CRSsNP, and CRSwNP without asthma. Co, controls; CS, CRSsNP; NP, CRSwNP; NP+Asth, CRSwNP and asthma.


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