Abstract
Abstract Aspergillus fumigatus is a mold fungal pathogen and the most common cause of invasive aspergillosis (IA), a serious infection that develops in patients with compromised immune function. Although a variety of immune cells can help confer protection against IA, the mechanisms that govern immune cell cooperation culminating in the eradication of conidia and IA prevention are unclear. Using selective cell depletion strategies our recent studies have shown that, in addition to neutrophils, CCR2+ inflammatory monocytes (CCR2+Mo) and their derivative monocyte-derived dendritic cells (Mo-DCs) are required for the prevention of IA. In preliminary studies, we find that IA development in neutrophil-depleted animals is associated with diminished Mo-DC differentiation and lower conidiacidal activity in these cells. We hypothesize that neutrophil and CCR2+Mo functions are interdependent, continuously cross-regulating each other’s antifungal activities. We are currently investigating the mechanisms of CCR2+Mo and neutrophil cross-regulation, and characterizing their overall contributions to anti-fungal immunity.
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