Local receptor revision and class switching to IgE in chronic rhinosinusitis with nasal polyps

Gevaert, Philippe; Nouri‐Aria, Kayhan T.; Wu, Hui‐Fen; Harper, Charles L.; Takhar, Pooja; Fear, David; Acke, Frederic; Ruyck, Natalie De; Banfield, G.; Kariyawasam, Harsha H.; Bachert, Claus; Durham, Stephen R.; Gould, Hannah J.

doi:10.1111/all.12054

Cited by 136 publications

(159 citation statements)

References 38 publications

(45 reference statements)

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“…However, IgE also can be produced from GC-independent sources, because B cell lymphoma 6-deficient or lymphotoxin-a-deficient mice produce IgE, despite having defective formation of GCs or lymph nodes, respectively (48,49). Furthermore, although local production of IgE in mucosal tissues is important in allergic disease, and some studies suggested the local formation of GC-like structures (50,51), it is not clear how GC responses are important for local IgE production (46). Our results demonstrate that MyD88 also may mediate GCindependent IgE production, if any, in lungs exposed to ragweed pollen, because IgE responses were totally abrogated in Myd88 2/2 mice.…”

Section: Discussionmentioning

confidence: 99%

B Cell–Intrinsic MyD88 Signaling Is Essential for IgE Responses in Lungs Exposed to Pollen Allergens

Matsushita

Yoshimoto

2014

The Journal of Immunology

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Allergen-specific IgE is linked to asthma pathogenesis, but the underlying mechanisms of IgE production in response to allergen exposure are poorly understood. In this article, we show that B cell–intrinsic MyD88 is essential for IgE/IgG1 production evoked by ragweed pollen instilled into lungs. MyD88-deficient mice showed defective IgE/IgG1 production and germinal center responses to lung instillation of ragweed pollen. However, MyD88 was dispensable for dendritic cell activation and Th2 cell development. B cell–specific deletion of MyD88 replicated the defective Ab production observed in MyD88-deficient mice. Although ragweed pollen contains TLR ligands, TLR2/4/9-deficient mice developed normal allergic responses to ragweed pollen. However, anti–IL-1R1 Ab-treated mice and IL-18–deficient mice showed decreased IgE/IgG1 production with normal Th2 development. Furthermore, B cell–specific MyD88-deficient mice showed reduced IgE/IgG1 production in response to lung instillation of OVA together with IL-1α, IL-1β, or IL-18. Thus, pollen instillation into lungs induces IL-1α/β and IL-18 production, which activates B cell–intrinsic MyD88 signaling to promote germinal center responses and IgE/IgG1 production.

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Section: Discussionmentioning

confidence: 99%

B Cell–Intrinsic MyD88 Signaling Is Essential for IgE Responses in Lungs Exposed to Pollen Allergens

Matsushita

Yoshimoto

2014

The Journal of Immunology

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“…913 Most importantly, IgE antibodies to enterotoxins (SE-IgE) were associated with significantly higher concentrations of IgG, specifically of the IgG4 subclass, and IgE in NPs. 914 In CRSwNP, evidence for local IgE synthesis and class switch recombination was also provided 915 ; recombination activating genes RAG1 and RAG2 mRNA concentrations were increased in polyps and correlated with the magnitude of inflammation and the presence of SE-specific IgE in the NP mucosa, pointing to a very active local Ig production in SEIgE positive polyps. The locally formed IgE is polyclonal, with IgE antibodies against several hundred or more allergens, and functional, even in the absence of systemic IgE antibodies or a positive skin-prick test.…”

Section: Viiib Crswnp: Comorbid Asthmamentioning

confidence: 99%

International Consensus Statement on Allergy and Rhinology: Rhinosinusitis

Orlandi

Kingdom

Hwang

et al. 2016

Int Forum Allergy Rhinol

557

888

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Background:The body of knowledge regarding rhinosinusitis (RS) continues to expand, with rapid growth in number of publications, yet substantial variability in the quality of those presentations. In an effort to both consolidate and critically appraise this information, rhinologic experts from around the world have produced the International Consensus Statement on Allergy and Rhinology: Rhinosinusitis (ICAR:RS). Methods:Evidence-based reviews with recommendations (EBRRs) were developed for scores of topics, using previously reported methodology. Where existing evidence was insufficient for an EBRR, an evidence-based review (EBR) was produced. The sections were then synthesized and the entire manuscript was then reviewed by all authors for consensus. Results:The resulting ICAR:RS document addresses multiple topics in RS, including acute RS (ARS), chronic RS (CRS) with and without nasal polyps (CRSwNP and CRSsNP), recurrent acute RS (RARS), acute exacerbation of CRS (AE-CRS), and pediatric RS. Conclusion:As a critical review of the RS literature, ICAR:RS provides a thorough review of pathophysiology and evidence-based recommendations for medical and surgical treatment. It also demonstrates the significant gaps in our understanding of the pathophysiology and optimal management of RS. Too o en the foundation upon which these recommendations are based is comprised of lowerlevel evidence. It is our hope that this summary of the evidence in RS will point out where additional research efforts may be directed. C 2016 ARS-AAOA, LLC. Key Words:rhinosinusitis; chronic rhinosinusitis; acute rhinosinusitis; recurrent acute rhinosinusitis; evidence-based medicine; systematic review; endoscopic sinus surgery List of Abbreviations Used

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“…84,85 Inflammatory response amplification via bacterial super-antigens is also observed and leads to enhanced nasal IgE production. 86 In contrast, CRSsNP is characterized by a distinct inflammatory pattern, with a Th1 cell bias and excess interferon-c (IFN-c) and neutrophilic inflammation. 87 Whilst both CRS phenotypes have a high incidence of lower airway disease with asthma and bronchiectasis, the poor ability to subtype CRSsNP inflammatory profiles makes it difficult to compare remodelling changes with those occurring in the lower airway.…”

Section: Ch Ronic R Hin Osin Usitis and Sinon Asal Remodellingmentioning

confidence: 99%

Upper and lower airway remodelling mechanisms in asthma, allergic rhinitis and chronic rhinosinusitis: The one airway concept revisited

Samitas

Carter

Kariyawasam

et al. 2017

Allergy

Self Cite

210

156

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Allergic rhinitis (AR), chronic rhinosinusitis (CRS) and asthma often co-exist. The one airway model proposes that disease mechanisms occurring in the upper airway may mirror lower airway events. Airway remodelling is the term used to describe tissue structural changes that occur in a disease setting and reflect the dynamic process of tissue restructuring during wound repair. Remodelling has been long identified in the lower airways in asthma and is characterized by epithelial shedding, goblet cell hyperplasia, basement membrane thickening, subepithelial fibrosis, airway smooth muscle hyperplasia and increased angiogenesis. The concept of upper airway remodelling has only recently been introduced, and data so far are limited and often conflicting, an indication that more detailed studies are needed. Whilst remodelling changes in AR are limited, CRS phenotypes demonstrate epithelial hyperplasia, increased matrix deposition and degradation along with accumulation of plasma proteins. Despite extensive research over the past years, the precise cellular and molecular mechanisms involved in airway remodelling remain incompletely defined. This review describes our current rather limited understanding of airway remodelling processes in AR, CRS and asthma and presents mechanisms both shared and distinct between the upper and lower airways. Delineation of shared and disease-specific pathogenic mechanisms of remodelling between the sinonasal system and the lung may guide the rational design of more effective therapeutic strategies targeting upper and lower airways concomitantly and improving the health of individuals with inflammatory airway diseases.

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Local receptor revision and class switching to IgE in chronic rhinosinusitis with nasal polyps

Abstract: Our results provide the first evidence of local receptor revision and class switching to IgE, and B-cell differentiation into IgE-secreting plasma cells in NP.

Cited by 136 publications

References 38 publications

B Cell–Intrinsic MyD88 Signaling Is Essential for IgE Responses in Lungs Exposed to Pollen Allergens

B Cell–Intrinsic MyD88 Signaling Is Essential for IgE Responses in Lungs Exposed to Pollen Allergens

International Consensus Statement on Allergy and Rhinology: Rhinosinusitis

Upper and lower airway remodelling mechanisms in asthma, allergic rhinitis and chronic rhinosinusitis: The one airway concept revisited

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