Abstract
Mucosal immune responses to C. albicans are highly diverse because of the variety of fungal PAMPs and antigens recognised by different host cells at multiple infection sites. The key function of epithelial cells appears to be discrimination between the morphological status and between the potentially commensal and pathogenic states of C. albicans. Epithelial activation initiates a complex network of immune interactions between host and fungus, which determines the downstream innate and adaptive response that ultimately resolves the infection. Whilst much progress has been made in deciphering the key proteins, cells, and mechanisms contributing to host immunity against Candida, the next few years should provide a leap forward in clinical and translational applications with regard to how Candida infections can be managed and controlled at mucosal surfaces without recourse to antimycotic agents.
Highlights
Mucosal immune responses to C. albicans are highly diverse because of the variety of fungal PAMPs and antigens recognised by different host cells at multiple infection sites
Epithelial activation initiates a complex network of immune interactions between host and fungus, which determines the downstream innate and adaptive response that resolves the infection
Deciphering the key proteins, cells, and mechanisms contributing to host immunity against Candida, the few years should provide a leap forward in clinical and translational applications with regard to how Candida infections can be managed and controlled at mucosal surfaces without recourse to antimycotic agents
Summary
Mucosal and Salivary Biology Division, King's College London Dental Institute, King's College London, London, United Kingdom. Candida species are one of the most common fungal pathogens of humans and the causative agents of superficial and invasive candidiasis. The vast majority of Candida infections are mucosal, manifesting as vaginal or oral candidiasis, which together account for an estimated 40 million infections per year. High-level Candida colonisation is associated with several gut diseases, including Crohn's disease and ulcerative colitis, and reducing fungal burdens reduces disease severity [1]. Candida species are an ever-increasing problem in immunocompromised patients. In common with the vast majority of life-threatening systemic infections, systemic Candida infections are usually acquired through mucosal surfaces. It is of paramount importance to understand how epithelial tissues detect and restrict these pathogens to mucosal surfaces
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