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The Journal of Immunology, 2005, 174: 5024-5032.
Copyright © 2005 by The American Association of Immunologists

Allergen Drives Class Switching to IgE in the Nasal Mucosa in Allergic Rhinitis1

Pooja Takhar*, Lyn Smurthwaite*, Heather A. Coker*, David J. Fear*, Graham K. Banfield{dagger}, Victoria A. Carr{dagger}, Stephen R. Durham{dagger} and Hannah J. Gould2,*

* The Randall Division, King’s College London, London, United Kingdom; and {dagger} Upper Respiratory Medicine, Imperial College School of Medicine, National Heart and Lung Institute, London, United Kingdom

IgE-expressing B cells are over 1000 times more frequent in the nasal B cell than the peripheral blood B cell population. We have investigated the provenance of these B cells in the nasal mucosa in allergic rhinitis. It is generally accepted that expression of activation-induced cytidine deaminase and class switch recombination (CSR) occur in lymphoid tissue, implying that IgE-committed B cells must migrate through the circulation to the nasal mucosa. Our detection of mRNA for activation-induced cytidine, multiple germline gene transcripts, and {epsilon} circle transcripts in the nasal mucosa of allergic, in contrast to nonallergic control subjects, however, indicates that local CSR occurs in allergic rhinitis. The germline gene transcripts and {epsilon} circle transcripts in grass pollen-allergic subjects are up-regulated during the season and also when biopsies from allergic subjects are incubated with the allergen ex vivo. These results demonstrate that allergen stimulates local CSR to IgE, revealing a potential target for topical therapies in allergic rhinitis.




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