Complement factor C5 inhibition reduces type 2 responses without affecting group 2 innate lymphoid cells in a house dust mite induced murine asthma model.
Yang, Jack; Ramirez Moral, Ivan; van 't Veer, Cornelis; de Vos, Alex F; de Beer, Regina; Roelofs, Joris J T H; Morgan, B Paul; van der Poll, Tom.
; 20(1): 165, 2019 Jul 24.
Artigo em Inglês | MEDLINE | ID: mdl-31340811
House Dust Mite-Induced Allergic Airway Disease Is Independent of IgE and FcÎµRIα.
The interleukin-33 receptor ST2 is important for the development of peripheral airway hyperresponsiveness and inflammation in a house dust mite mouse model of asthma.
T cells are necessary for ILC2 activation in house dust mite-induced allergic airway inflammation in mice.
Pathophysiological features of asthma develop in parallel in house dust mite-exposed neonatal mice.
Development of eosinophilic inflammation is independent of B-T cell interaction in a chronic house dust mite-driven asthma model.
Acidic mammalian chitinase is not a critical target for allergic airway disease.
Peptidoglycan recognition protein 1 promotes house dust mite-induced airway inflammation in mice.
Vitamin E Isoform Î³-Tocotrienol Downregulates House Dust Mite-Induced Asthma.
Dynamics of IL-4 and IL-13 expression in the airways of sheep following allergen challenge.
IL-33 promotes the induction of immunoglobulin production after inhalation of house dust mite extract in mice.