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Mucosal Immunol. 2014 May;7(3):558-67. doi: 10.1038/mi.2013.74. Epub 2013 Oct 16.

Dectin-2 sensing of house dust mite is critical for the initiation of airway inflammation.

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Departments of Respiratory, Inflammation and Autoimmunity, MedImmune Ltd, Cambridge, UK.
Department of Pathology, Safety Assessment UK, AstraZeneca R&D, Loughborough, UK.
Research Histology, MedImmune Ltd, Cambridge, UK.
1] Departments of Respiratory, Inflammation and Autoimmunity, MedImmune Ltd, Cambridge, UK [2] Present address: Johnson & Johnson, London, UK.


How the immune system senses aeroallergens and triggers an aberrant inflammation is poorly understood. Dectin-2 is a house dust mite (HDM)-sensing pattern recognition receptor. In a 3-week mouse model of repeated intranasal HDM challenge, anti-Dectin-2 potently attenuated the characteristic allergic inflammation and airway hyper-responsiveness. Anti-Dectin-2 also prevented neutrophil influx following a single HDM challenge. Interestingly, cysteinyl leukotrienes, but not chemokine and cytokine levels were inhibited by anti-Dectin-2 in this acute model, and in ex vivo challenge of cultured alveolar macrophages with HDM. Furthermore in the single-challenge model, zileuton, an inhibitor of leukotriene production, produced a similar effect as Dectin-2 blockade. Together these data suggest alveolar macrophage sensing of HDM by Dectin-2 elicits the production of cysteinyl leukotrienes, and this axis is key for the initiation of airway inflammation to this aeroallergen. Finally, we found Dectin-2-positive infiltrating cells present in bronchial biopsies from asthmatic subjects.

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