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  Indian J Med Microbiol
 

Figure 1: Pathogenesis of allergic bronchopulmonary aspergillosis. Aspergillus conidia trapped in the airway mucus germinate into hyphae, in genetically predisposed individuals. The hyphae provide the antigenic stimulus for the allergic response, resulting in fungal sensitization. In susceptible individuals, an exaggerated T-helper 2 (Th2) immune response promotes further airway inflammation. This phase is characterized by recruitment of mast cells, increased production of immunoglobulin E (total as well as specific IgE to the fungus) and IgG antibodies to the fungi. The secreted chemokines and cytokines attract large number of eosinophils which attack the fungal hyphae, perpetuate further inflammation, finally culminating in end-organ damage and clinical manifestations. The red arrows indicate the steps where genetic predisposition plays a key role.

Figure 1: Pathogenesis of allergic bronchopulmonary aspergillosis. <i>Aspergillus</i> conidia trapped in the airway mucus germinate into hyphae, in genetically predisposed individuals. The hyphae provide the antigenic stimulus for the allergic response, resulting in fungal sensitization. In susceptible individuals, an exaggerated T-helper 2 (Th2) immune response promotes further airway inflammation. This phase is characterized by recruitment of mast cells, increased production of immunoglobulin E (total as well as specific IgE to the fungus) and IgG antibodies to the fungi. The secreted chemokines and cytokines attract large number of eosinophils which attack the fungal hyphae, perpetuate further inflammation, finally culminating in end-organ damage and clinical manifestations. The red arrows indicate the steps where genetic predisposition plays a key role.