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Food allergen‐sensitized CCR 9 + lymphocytes enhance airways allergic inflammation in mice
Author(s) -
Castan L.,
Cheminant M.A.,
Colas L.,
Brouard S.,
Magnan A.,
Bouchaud G.
Publication year - 2018
Publication title -
allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.363
H-Index - 173
eISSN - 1398-9995
pISSN - 0105-4538
DOI - 10.1111/all.13386
Subject(s) - immunology , allergy , food allergy , medicine , allergic inflammation , house dust mite , inflammation , asthma , immune system , homing (biology) , allergic response , allergen , chemokine , immunoglobulin e , biology , antibody , ecology
Abstract Background The mechanisms of the atopic march, characterized by a natural progression from food and cutaneous allergies to rhinitis and asthma, are still unknown. However, as several organs can be involved, chemokines and their receptors might be implicated in this process and may be instrumental factors. Objectives We hypothesized that the T‐cell gut‐homing receptor CCR 9 could be implicated in the evolution of allergic diseases. Methods We characterized the immune response and the role of CCR 9 in a murine model combining food allergy to wheat gliadin and a model of acute airways inflammation in response to house dust mite. Results Compared with solely asthmatic‐like mice, we demonstrated that the aggravation of pulmonary symptoms in consecutive food and respiratory allergies, characterized by an increase in pulmonary resistance and a higher Th17/Treg ratio, was abrogated in CCR 9 knockout mice. Moreover, transfer of food‐allergic CD 4 + T cells from wild‐type but not from CCR 9 −/− aggravated airways inflammation demonstrating that CCR 9 is involved in food allergy‐enhanced allergic airway inflammation to unrelated allergens. Conclusion Taken together, our results demonstrated a crucial role of the T‐cell homing receptor CCR 9 in this model and validated its potential for use in the development of therapeutic strategies for allergic diseases.