Localized immunoglobulin E expression in allergic rhinitis and nasal polyposis

Wise, Sarah K.; Ahn, Chadwick N; Schlosser, Rodney J.

doi:10.1097/moo.0b013e32832ad23d

Cited by 37 publications

(31 citation statements)

References 38 publications

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“…Interleukin (IL)-4, IL-13, and CD40, the necessary elements for IgE production, also have been detected within sinonasal tissue. Inferior turbinate tissue from patients with known allergy to grass pollen was studied after antigen exposure in vitro and found to have an increase in IL-4 RNA and germline ε gene exons, which are spliced out during immunoglobulin class-switching gene recombination [33,34]. Takhar et al [35] showed that both in vitro and in vivo exposure to grass pollen in allergic patients stimulates production of circle transcripts, a marker of ongoing class-switching, and that class-switch recombination to IgE from multiple other isotypes occurs in the sinonasal mucosa.…”

Section: Initial Studies Of Local Ige In the Airwaysmentioning

confidence: 99%

The Role of IgE Production in the Pathophysiology of Rhinitis and Rhinosinusitis

Hoddeson

Wise

2011

Curr Allergy Asthma Rep

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A multitude of potential etiologies exist for rhinitis and rhinosinusitis. These sinonasal disorders are heterogeneous entities that are best understood by evaluating the causative factors in each individual patient. More precise diagnosis permits accurate and effective treatment. The association of allergy with sinonasal symptoms has been described for decades; however, the specific relationship between allergy, rhinitis, and rhinosinusitis is complex. Considering allergy in terms of a systemic atopic disorder, along with a local inflammatory process mediated by IgE production in sinonasal tissues, is helpful in unveiling the complex connection between allergy, rhinitis, and rhinosinusitis. This article reviews recent literature regarding local IgE and sinonasal inflammatory conditions.

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Section: Initial Studies Of Local Ige In the Airwaysmentioning

confidence: 99%

The Role of IgE Production in the Pathophysiology of Rhinitis and Rhinosinusitis

Hoddeson

Wise

2011

Curr Allergy Asthma Rep

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“…Clinical studies have found a close association between asthma and serum IgE levels, and the amount of allergen-specific IgE can be dramatically increased in sensitized or atopy patients (7,8). Allergen-specific IgE is located in the human airway, such as in nasal mucosa from allergic patients who suffer allergic rhinitis in sinonasal tissue, nasal polyposis, and allergic fungal rhinosinusitis (9)(10)(11)(12). This observation is further supported by the fact that B cells from the nasal mucosa of allergic individuals locally synthesize IgE (13,14).…”

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confidence: 99%

CD23-Dependent Transcytosis of IgE and Immune Complex across the Polarized Human Respiratory Epithelial Cells

Palaniyandi

Tomei

et al. 2011

The Journal of Immunology

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IgE-mediated allergic inflammation occurs when allergens cross-link IgE on the surface of immune cells, thereby triggering the release of inflammatory mediators as well as enhancing Ag presentations. IgE is frequently present in airway secretions, and its level can be enhanced in human patients with allergic rhinitis and bronchial asthma. However, it remains completely unknown how IgE appears in the airway secretions. In this study, we show that CD23 (FcεRII) is constitutively expressed in established or primary human airway epithelial cells, and its expression is significantly upregulated when airway epithelial cells were subjected to IL-4 stimulation. In a transcytosis assay, human IgE or IgE-derived immune complex (IC) was transported across a polarized Calu-3 monolayer. Exposure of the Calu-3 monolayer to IL-4 stimulation also enhanced the transcytosis of either human IgE or the IC. A CD23-specific Ab or soluble CD23 significantly reduced the efficiency of IgE or IC transcytosis, suggesting a specific receptor-mediated transport by CD23. Transcytosis of both IgE and the IC was further verified in primary human airway epithelial cell monolayers. Furthermore, the transcytosed Ag–IgE complexes were competent in inducing degranulation of the cultured human mast cells. Because airway epithelial cells are the first cell layer to come into contact with inhaled allergens, our study implies CD23-mediated IgE transcytosis in human airway epithelial cells may play a critical role in initiating and contributing to the perpetuation of airway allergic inflammation.

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“…Patients with AFRS frequently exhibit positive reactions to multiple fungal and nonfungal antigens, guiding subsequent allergen-specific immunotherapy. 32,[37][38][39][40][41] There is a subset of patients, however, who demonstrate the classic features of AFRS, but do not exhibit elevated systemic levels of total IgE. 32,42 In a 2004 study, Collins and colleagues 43 investigated a phenomenon termed ''entopy,'' or increased local IgE in the absence of systemic disease in AFRS.…”

Section: Local Ige: Intranasal Elevated Ige In Nasal Tissuesmentioning

confidence: 97%

“…31 In 1970, Tse and colleagues demonstrated ragweed-specific IgE in nasal washings of ragweed-allergic patients with allergic rhinitis, providing additional evidence for local antigen-specific IgE in nasal mucosa. [31][32][33] In a 1974 study by Huggins and Brostoff, 34 patients with typical allergic rhinitis symptoms with both positive and negative systemic allergy tests, as well as patients free from any allergic symptoms, were exposed to grasspollen extract intranasally. Subsequent nasal washings revealed elevated grass pollen-specific IgE in all patients with allergic rhinitis regardless of systemic allergy test status, when compared with nonallergic controls, suggesting local intranasal IgE production.…”

Section: Local Ige: Intranasal Elevated Ige In Nasal Tissuesmentioning

confidence: 99%