作者: Lauren Folgosa Cooley , Rebecca K. Martin , Hannah B. Zellner , Anne-Marie Irani , Cora Uram-Tuculescu
DOI: 10.1371/JOURNAL.PONE.0124331
关键词:
摘要: ADAM10, as the sheddase of low affinity IgE receptor (CD23), promotes production and thus is a unique target for attenuating allergic disease. Herein, we describe that B cell levels specifically, are increased in patients Th2 prone WT mouse strains (Balb/c A/J). While T help augments ADAM10 expression, Balb cells exhibit naive state even more dramatically after anti-CD40/IL4 stimulation compared C57 (Th1 prone) cells. Furthermore, ADAM17 TNF reduced A/J) to Th1 controls. To further understand this regulation, were studied C57Bl/6 Balb/c mice deficient ADAM10. C57-ADAM10B-/- adept at increasing cleavage resulting excess follicular abnormal secondary lymphoid tissue architecture not noted Balb-ADAM10B-/-. Moreover, level well Th context critical determining potential. Using murine house dust mite airway hypersensitivity model, high WT) optimal disease induction including bronchoconstriction, goblet metaplasia, mucus, inflammatory cellular infiltration, production. have attenuated lung symptoms actually most similar prone). symptomology. Taken together, it consider both innate when host susceptibility High would diagnostically predicting susceptibility; and, provide support use inhibitors treating