Endothelial amine oxidase AOC3 transiently contributes to adaptive immune responses in the airways |
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| Authors: | Markus Ollert Helmut Fuchs Valerie Gailus‐Durner Martin Hrabě de Angelis Sirpa Jalkanen Tibor Z. Veres |
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| Affiliation: | 1. Department of Dermatology and Allergy, Klinikum rechts der Isar, Biederstein, Technische Universit?t München (TUM), Munich, Germany;2. Clinical, Research Group Molecular Allergology, Center of Allergy and Environment Munich (ZAUM), Technische Universit?t München (TUM), and Institute for Allergy Research, Helmholtz Zentrum München, German Research Center for Environmental Health, Munich‐Neuherberg, Germany;3. German Mouse Clinic, Helmholtz Zentrum München, German Research Center for Environmental Health, Neuherberg, Germany;4. Institute for Experimental Genetics, Helmholtz Zentrum München, German Research Center for Environmental Health, Neuherberg, Germany;5. Department of Experimental Genetics, Center of Life and Food Sciences Weihenstephan, Technische Universit?t München, Freising‐Weihenstephan, Germany;6. Medicity Research Laboratory, University of Turku, Turku, Finland;7. Department of Medical Microbiology and Immunology, University of Turku, Turku, Finland |
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| Abstract: | 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. |
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| Keywords: | Adaptive immunity Adhesion molecules Airways Allergy Leukocyte trafficking |
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