Allergic bronchopulmonary aspergillosis (ABPA) is a hypersensitivity lung disease caused predominantly by the ubiquitous fungus Aspergillus fumigatus. ABPA is characterized by eosinophilia, fleeting pulmonary infiltrates, central bronchiectasis, elevated serum IgE and Aspergillus specific IgG and IgE. The pathogenetic mechanism implicated in ABPA is not completely understood. The cytokine response detected in ABPA patients is of a CD4+ Th2 type as evidenced by the production of IL-4, IL-5, and very little or no IFN-g on stimulation of T-lymphocytes with Aspergillus antigens. Animal model studies using wild type and gene knockout mice indicate a more precise mechanism of lung injury in antigen exposed animals. IL-4 knockout mice invariably showed a predominant Th1 response. B-cell deficient and IgE knockout mice exposed to A. fumigatus antigens showed airway response similar to wild type mice indicating a lesser role for IgE and other antibodies in the pathogenesis of murine experimental ABPA. RAG negative mice failed to show airway hyperreactivity response, although airway hyperreactivity was induced in naive RAG negative animals when T-cells from wild type Aspergillus immunized mice were transferred. The results of these studies indicate a multi-factorial immunopathogenesis in ABPA, which include T-cells, IgE, eosinophils, mast cells, and various cytokines and chemokines.