Although the mechanisms underlying DC-SIGN-mediated immune response are still highly speculative, it has been suggested that DC-SIGN promotes dendritic cell (DC) migration and T-cell activation through the ICAM-3 binding [12, 13] and modulates TLR signalling by targeting Raf-1, which regulates NFkB p65 activation and, consequently the production of pro-inflammatory cytokines [14] . Likewise, Dectin-1 and Dectin-2 induce Sykdependent canonical and noncanonical NFkB pathways [15, 16] promoting the production of some pro-inflammatory cytokines (IL1a, IL1b, IL12 and IL8), chemokines (CCL2/MCP-1, CCL3/ MIP-1, CXCL2/MIP-2 and CXCL10) [17] and the IL17-mediated neutrophil recruitment [18] . It has also been described that Dectin-1 and Dectin-2 are able to work in collaboration with TLRs (mainly TLR2, TLR4 and TLR6) modulating immune responses through the production of IL6, IL12p70 and TNF [3, 16] . These findings support the hypothesis that C-type lectins, cytokines or chemokines are important mediators during infection with A. fumigatus.