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Sorting out host recognition of fungal infection (FUNGISORT)
Start date: Jun 1, 2014, End date: May 31, 2016 PROJECT  FINISHED 

The fungus Candida albicans is a common cause of human infection with serious morbidity, but the organism is also a commensal yeast that is part of the normal gut microbiota. It is becoming increasingly clear that the composition of the microbiome plays an important role in health and disease. For instance, recently it was shown that commensal fungi in the gut can contribute to the severity of colitis (inflammation of the gut). Immune recognition of C. albicans is mediated by Pattern Recognition Receptors (PRRs) of innate immune cells. The major PRRs involved in fungal immune responses are C-type lectin receptors Dectin-1, DC-SIGN, Dectin-2, Mincle, Galectin-3 and Mannose Receptor. Signaling by C-type lectin receptors depends on the formation of signaling protein complexes, but these complexes are poorly characterized. We need to understand C-type lectin-mediated immune responses to fungi to improve diagnostics and generate new anti-fungal drugs and vaccines. My approach to increase our understanding of fungal immune recognition is to (1) Characterize C-type lectin receptor complexes that drive innate recognition of C. albicans using sortase technology (2) Study immune recognition of commensal and pathogenic Candida strains and isolates with fluorescent PRR binding domains and (3) Investigate the contribution of fungi to the development and/or severity of human inflammatory bowel disease (IBD) by quantitative proteomics. Fungal infections are on the rise so we need to understand how the immune system detects pathogenic behavior of commensal fungi. My expertise in the fungal host-pathogen field and the advanced technologies that I have developed put me in a unique position to advance our understanding of immune-fungal interactions. The results of this IIF project will offer a clear perspective on future clinical applications.

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