“…A.f conidia into mice significantly decreases the immune response (CXCL1/KC, TNF-alpha, CCL3/MIP-1, IL-6, and GM-CSF) and results in much higher fungal burdens (Steele et al, 2005). Secondly, the exposed β-glucan bound by a mIgG Fc portion fused to Dectin-1 targets the microbe for enhanced clearance via Fc binding receptors, this decreased fungal burden and enhanced survival of the infected mice (Mattila et al, 2008;Rodriguez-de la Noval et al, 2020). The aspergillus GAG layer masks the β-glucan layer as can be observed with the Δuge3 mutant, lacking GalNAc, has increased binding to FcDectin-1 on both swollen conidia and hyphae, and the mutant is less virulent due to the increased detection of the exposed β-glucan by the immune system (Gravelat et al, 2013).…”