Abstract
Among the several human fungal pathogens, Candida genus represents one of the most implicated in the clinical scenario. There exist several distinctive features that govern the establishment of Candida infections in addition to their capacity to adapt to multiple stress conditions inside humans which also include evasion of host immune responses. The complex fungal cell wall of the prevalent pathogen, Candida albicans, is one of the main targets of antifungal drugs and recognized by host immune cells. The wall consists of tiered arrangement of an outer thin but dense covering of mannan and inner buried layers of β-glucan and chitin. However, the pathogenic fungi adopt strategies to evade immune recognition by masking these molecules. This capacity to camouflage the immunogenic polysaccharide β-glucan from the host is a key virulence factor of C. albicans. The present review is an attempt to collate various underlying factors and mechanisms involved in Candida β-glucan masking from the available pool of knowledge and provide a comprehensive understanding. This will further improve therapeutic approaches to candidiasis by identifying new antifungal targets that blocks fungal immune evasion.
Highlights
Human fungal infections, due to Candida species, are the foremost source of nosocomial life-threatening infections
Since Dectin-1 signaling is ligand size-dependent, masked β-glucan exposures may be limited to non-stimulatory sizes, while unmasking processes may result in larger β-glucan exposures that are more effective at activating Dectin-1
Given the prevalent multidrug resistance (MDR) scenario in Candida spp., boosting of the immune response by exposing factors manipulating the β-glucan masking phenomenon endorsed in this review presents an alternative approach that needs attention (Table 1)
Summary
Due to Candida species, are the foremost source of nosocomial life-threatening infections. The ability of Candida to express virulence traits marks the success of the pathogen to cause pathogenicity These virulence factors include biofilm formation, cell adhesins, hyphal formation, phenotypic switching, exoenzymatic activity (phospholipase, proteinase), and hemolysin production along with immune evasion [4]. To sense and adapt to the hostile niches and evade the immune responses is the basis of infectivity for any fungal pathogen affecting humans, including C. albicans. In this context, the cell wall is a necessary. The pathogen adopts strategies to evade immune recognition by masking these molecules This masking of β-glucan polysaccharides from immune detection is a key virulence factor of C. albicans. Any disturbances in the production and assembly of cell surface architecture lead to glucan layer unmasking, thereby increasing the susceptibility of the fungal pathogen to immune cells [9]
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