Opportunistic infections represent a major cause of non-relapse morbidity and mortality in patients with hematologic malignancies and in recipients of hematopoietic cell transplants. Invasive fungal infections are notoriously difficult to diagnose and treat in patients with compromised immune function and can postpone or interfere with potentially curative therapeutic interventions.
My laboratory research program focuses on human pathogenic fungi (Aspergillus fumigatus, Candida albicans, Cryptococcus neoformans) and dissects molecular and cellular mechanisms of sterilizing antifungal immunity, primarily in mouse models. We have developed innovative, fluorescence-based tools to measure the outcome of fungal cell – host cell encounters with single event resolution in the lung. Using transgenic mice that enable us to ablate, to label, or to delete genes in a conditional manner in monocytes, we have characterized the function of a novel innate immune effector cell during experimental challenges with fungal pathogens.
Current work in the laboratory focuses on identifying the molecular signals and effectors that enable fungal recognition, innate immune activation and crosstalk, and fungal killing in the lung as well as the role of endogenous fungal communities in immune homeostasis and regulation. On the clinical side, we strive to improve diagnostic approaches for invasive mycoses and to define genetic risk for fungal susceptibility in the context of hematopoietic cell transplantation. Our goal is to advance novel insight into these processes and enhance clinical outcomes in vulnerable patient groups.