Nasal mast cells in perennial allergic rhinitics exhibit increased expression of the Fc epsilonRI, CD40L, IL-4, and IL-13, and can induce IgE synthesis in B cells.
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Cross-linking of allergen specific IgE bound to the high affinity IgE receptor (Fc ⑀ RI) on the surface of mast cells with multivalent allergens results in the release of both preformed and newly generated mediators, and in the manifestation of allergic symptoms.The expression of Fc ⑀ RI, and the synthesis of IgE are therefore critical for the development of allergic diseases.In this study, we report that nasal mast cells (NMC) from patients with perennial allergic rhinitis (PAR) expressed significantly greater levels of the Fc ⑀ RI, CD40L, IL-4, and IL-13 as compared to NMC from patients with chronic infective rhinitis (CIR).The level of Fc ⑀ RI expression in NMC of PAR patients strongly correlated with the levels of serum total ( r ϭ 0.8, P Ͻ 0.003) and specific IgE ( r ϭ 0.89, P Ͻ 0.0004) antibodies.In addition, stimulation of NMC with IL-4, upregulated the Fc ⑀ RI ␣ chain expression both at the protein and mRNA levels, as detected by flow cytometry and reverse transcriptase-polymerase chain reaction.Furthermore, NMC from PAR, but not CIR, patients induced IgE synthesis by purified B cells in the presence of Der fII (mite antigen).These results suggest novel and critical roles for mast cells in promoting the allergic reaction through the increased expression of Fc ⑀ RI and by enhancing and amplifying the IgE production, within the local microenvironment.( J. Clin.Invest.1997.99:1492-1499.)Key words: Fc receptor • allergy • mast cells • IgE • Fc ⑀ RI MethodsPatient profile.40 patients with PAR (M/F ϭ 25:15; mean age: 23.2 Ϯ 8.2 yr), and 25 non-atopics with CIR (M/F ϭ 12:13; mean age: 33.2 Ϯ 11.8 yr) were selected after careful screening.All PAR patients were symptomatic, had positive Radioallergosorbent tests (RAST: grades 3-6) to house dust mite, (negative RAST to 16 other inhaled allergens tested), had no associated atopic disease, had not received immunotherapy, and were not taking steroids for at least 1 mo prior
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This results in increased production of immunomodulatory cytokines and chemical mediators, forming a positive-feedback amplification loop involving the IgE-IgE receptor cascade that perpetuates ongoing inflammation.
“This results in an increased production of immunomodulatory cytokines and chemical mediators, forming an important positive-feedback amplification loop involving the IgE-IgE receptor cascade, thus perpetuating ongoing inflammation.285,286”
From International Consensus Statement on Allergy and Rhinology: Allergic Rhinitis (2018) · cites this paper as [286]
The Introduction describes IgE–FcεRI binding as triggering release of cytokines and chemical mediators, and the Results report that IL-4 increases FcεRI expression. The Discussion suggests that nasal mast cells amplify IgE synthesis and thereby perpetuate chronic allergic inflammation. The paper thus supports the proposed amplification mechanism, but does not establish the positive-feedback loop or increased chemical-mediator production as demonstrated outcomes. (LLM, conf=0.84)
Experimental — accuracy not yet measuredIL-13 from mast cells plays a crucial role in mast cell-induced local IgE synthesis by B cells, which in turn upregulate FcεRI expression on mast cells.
“IL-13 from mast cells plays a crucial role in mast cell–induced local IgE synthesis by B cells,286,395 which in turn upregulate FcεRI expression on mast cells.286”
From International Consensus Statement on Allergy and Rhinology: Allergic Rhinitis (2018) · cites this paper as [286]
The Discussion reports that blocking IL-13 completely inhibited nasal mast cell–induced IgE synthesis in B cells, supporting the first clause. The Results and Abstract report a correlation between serum IgE and mast-cell FcεRI expression, but do not show that B-cell-produced IgE upregulates that receptor; the demonstrated upregulator was IL-4. Passage page numbers are unavailable in our copy. (LLM, conf=0.87)
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- Authors
- Pawankar, R., Okuda, M., Yssel, H., Okumura, K., & Ra, C.
- Affiliations
- Juntendo University (JP)
- Nippon Medical School (JP)
- Venue
- Journal of Clinical Investigation
- Published
- 1997-04-01
- Volume
- 99
- Issue
- 7
- Pages
- 1492-1499
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC507968
- OpenAlex
- W2021475285
- Cited by
- 340
- References
- 38
- Citations by year
- 2026: 1 · 2025: 5 · 2024: 2 · 2023: 7 · 2022: 6 · 2021: 7 · 2020: 5 · 2019: 5 · 2018: 10 · 2017: 6 · 2016: 8 · 2015: 13 · 2014: 11 · 2013: 7 · 2012: 10
- FWCI
- 9.02
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Mast cells and histamine
- Health Sciences › Medicine › Immunology and Allergy › Allergic Rhinitis and Sensitization
- Health Sciences › Medicine › Physiology › Asthma and respiratory diseases
- Keywords
- perennial allergic rhinitis, FcεRI, high-affinity IgE receptor, CD40 ligand, IL-4, IL-13, IgE production, B cells, house dust mites, specific IgE, receptor up-regulation, allergic inflammation, local microenvironment, mast cell activation
- MeSH terms
- Adult, B-Lymphocytes, Female, Rhinitis, Allergic, Seasonal, Humans, Immunoglobulin E, Male, Mast Cells, Membrane Glycoproteins, Nose, Interleukin-4, Receptors, IgE, Interleukin-13, CD40 Ligand
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