Early recognition of A. fumigatus by myeloid leukocytes is a crucial for down-stream immune response and conidia clearance and, therefore, in the development and progression of IPA infection [3] . Myeloid leukocytes are activated by patternrecognition receptors (PRRs), which directly recognize fungal cell wall structures and pathogen-associated molecular patterns (PAMPs) [4] . Among the PRRs expressed in neutrophils, pulmonary macrophages and dendritic cells, C-type lectin family members such as DC-SIGN (Dendritic Cell-Specific Intercellular adhesion molecule-3-Grabbing Non-integrin), Dectin-1 (Dendritic cell-associated C-type lectin-1) and Dectin-2 (Dendritic cellassociated C-type lectin-2) seem to be important in the effectiveness of innate immune response against A. fumigatus [5, 6] . Recent studies have reported that the C-type lectins mediate A. Fumigatus recognition, capture and internalization [7] and that their binding to fungal cell wall carbohydrates is highly specific and selective [8] . DC-SIGN and Dectin-1 recognize b-(1-3)-glucans and galactomannans (GM) in the cell wall of A. fumigatus [7, 9] while Dectin-2 interacts with a-mannans [10] . However, numerous studies have shown that C-type lectins are not only involved in the recognition of fungal pathogens but also in the induction of antifungal Th1 and Th17 immune responses [5, 11] .