An Adenoviral Vector Encoding Full-Length Dectin-1 Promotes Aspergillus-Induced Innate Immune Response in Macrophages

Introduction The incidence of invasive pulmonary aspergillosis (IPA) has increased significantly over the last two decades. Alveolar macrophages (AMs) represent the first line of pulmonary host response to Aspergillus conidia. Recognition of conidia by AMs involves Dectin-1 (CLEC7A), which is a conserved structure to combine β-glucans. The deficiency of Dectin-1 results in impaired fungal killing and uncontrolled growth of Aspergillus fumigatus. Thus, we hypothesized that high expression of Dectin-1 would enhance the host recognition and fungal killing.