IL-33, IL-25 and TSLP contribute to development of fungal-associated protease-induced innate-type airway inflammation

摘要: Certain proteases derived from house dust mites and plants are considered to trigger initiation of allergic airway inflammation by disrupting tight junctions between epithelial cells. It is known that inhalation such as mite-derived Der p1 and/or papaya-derived papain caused eosinophilia in naive mice even Rag-deficient lack acquired immune cells T, B NKT In contrast, little regarding the possible involvement Aspergillus species (fungal-associated proteases; FAP), which ubiquitous saprophytic fungi environment, development eosinophilia. Here, we found FAP led was dependent on protease-activated receptor-2 (PAR2), but not TLR2 TLR4. Those findings suggest protease activity FAP, endotoxins important setting. addition, mediated innate (ILCs) lymphoid cells, Whereas IL-33, IL-25 thymic stromal lymphopoietin (TSLP) involved induction FAP-induced ILC-mediated eosinophilia, IL-33—rather than TSLP—was critical for our model. Our improve understanding molecular mechanisms FAP.