Premium
IL ‐5 production by resident mucosal allergen‐specific T cells in an explant model of allergic rhinitis
Author(s) -
Skrindo I.,
Ballke C.,
Gran E.,
Johansen F.E.,
Baekkevold E. S.,
Jahnsen F. L.
Publication year - 2015
Publication title -
clinical and experimental allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.462
H-Index - 154
eISSN - 1365-2222
pISSN - 0954-7894
DOI - 10.1111/cea.12543
Subject(s) - allergen , explant culture , immunology , medicine , allergy , chemistry , in vitro , biochemistry
Summary Background Seasonal allergic rhinitis is a chronic inflammation in the nasal mucosa triggered by inhaled aeroallergens. The inflammatory reaction is controlled by allergen‐specific T cells, but where and how these T cells become activated is not fully understood. Objectives We wanted to determine whether allergen‐specific T‐helper (Th) 2 cells are residing in the nasal mucosa under steady‐state conditions outside of the pollen season and, if so, whether these cells are activated locally in response to allergen challenge. Methods Mucosal biopsies from the lower turbinate were obtained out of season from patients with either birch‐ or grass‐pollen‐allergic rhinitis and from healthy controls. Cultured explant samples were challenged with relevant pollen extract or with a mix of overlapping 20‐mer peptides derived from the sequence of the major birch allergen, Betula verrucosa (Bet v) 1. After 24 h, culture medium was harvested for multiplex cytokine and tryptase analysis. Results Significant amounts of interleukin ( IL )‐5 were secreted from resident cells in response to ex vivo allergen challenge in the allergic group only. No increase was observed for the other cytokines measured. Production of IL ‐5 in response to both extract and the Bet v1‐derived peptide mix strongly suggested that T cells were a major source of IL ‐5. Conclusion Our explant model indicated that local presentation of antigen to resident allergen‐specific Th2 cells is the early event in the pathogenesis of allergic rhinitis. These findings identify possible cellular targets for anti‐inflammatory treatment.