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Endothelial amine oxidase AOC3 transiently contributes to adaptive immune responses in the airways
Author(s) -
Dunkel Johannes,
AguilarPimentel Juan Antonio,
Ollert Markus,
Fuchs Helmut,
GailusDurner Valerie,
de Angelis Martin Hrabě,
Jalkanen Sirpa,
Salmi Marko,
Veres Tibor Z.
Publication year - 2014
Publication title -
european journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.272
H-Index - 201
eISSN - 1521-4141
pISSN - 0014-2980
DOI - 10.1002/eji.201444563
Subject(s) - immunology , biology , immune system , eosinophil , extravasation , priming (agriculture) , lymphatic system , lymph , antigen , high endothelial venules , pathology , asthma , medicine , botany , germination
Amine oxidase, copper containing 3 (AOC3, also known as vascular adhesion protein‐1 (VAP‐1)) is an endothelial adhesion molecule that contributes to the extravasation of neutrophils, macrophages, and lymphocytes to sites of inflammation. However, the role of AOC3/VAP‐1 in allergic responses remains unknown. Here, we studied eosinophil and CD4 + T‐cell recruitment to the airways using AOC3/VAP‐1‐deficient mice. In an OVA‐triggered asthma model, AOC3/VAP‐1 slightly contributed to the accumulation of leukocytes in lungs in an age‐dependent manner. We then established a new model to kinetically measure recruitment of OVA‐specific CD4 + T cells to different airway immune compartments during the priming and effector phases of an adaptive immune response. The results showed that in the absence of AOC3/VAP‐1, recruitment of antigen‐specific CD4 + T cells to draining bronchial lymph nodes is reduced by 89% on day 3 after tracheal allergen exposure, but this difference was not observed on day 6. The dispersal of effector cells to lung and tracheal mucosa is AOC3/VAP‐1 independent. Thus, in allergic airway reactions, AOC3/VAP‐1 transiently contributes to the antigen‐specific, CD4 + T‐cell traffic to secondary lymphatic tissues, but not to airway mucosa or lung parenchyma. Our results suggest a largely redundant function for AOC3/VAP‐1 in allergic inflammatory responses of the airways.