摘要: Allergic bronchopulmonary aspergillosis (ABPA) is a hypersensitivity lung disease mediated by an allergic late-phase inflammatory response to Aspergillus fumigatus antigens. ABPA characterized markedly elevated Aspergillus-specific and total IgE levels eosinophilia, manifested wheezing, pulmonary infiltrates bronchiectasis fibrosis, which affect asthmatic cystic fibrosis (CF) patients. In the pathogenesis of ABPA, A. proteases play role in facilitation antigen transport across epithelial cell layer damaging integrity direct interaction with surface receptors, resulting pro-inflammatory cytokine production corresponding responses. genetically susceptible CF patients, this leads allergens. A genetic susceptibility HLA-DR restriction demonstrated increased frequency HLA-DR2 and/or DR5 lack HLA-DQ2. IL-4 plays central development Our group has that patients have sensitivity stimulation skewing Th2 responses allergens subjects Th1 non-ABPA subjects. Interestingly, stimulate IL-10 synthesis both