Fungi can cause disease in humans, from mucocutaneous to life-threatening systemic infections. Initiation of antifungal immunity involves fungal recognition by pattern recognition receptors such as C-type lectin receptors (CLRs). These germline-encoded receptors trigger a multitude of innate responses including phagocytosis, fungal killing, and antigen presentation which can also shape the development of adaptive immunity. Recently, studies have shed light on how CLRs directly or indirectly modulate lymphocyte function. Moreover, CLR-mediated recognition of commensal fungi maintains homeostasis and prevents invasion from opportunistic commensals. We present an overview of current knowledge of antifungal T cell immune responses, with emphasis on the role of C-type lectins, and discuss how these receptors modulate these responses at different levels.
Highlights CLRs are essential pattern recognition receptors involved in fungal recognition and initiation of protective antifungal immunity. CLRs promote the differentiation of mammalian T helper cell subsets essential for the control of systemic (Th1) and mucosal (Th17) fungal infections. CLRs are involved in antigen presentation, the expression of co-stimulatory molecules, and cytokine secretion; therefore, they can regulate lymphocyte function and adaptive immune responses at different levels. Fungal morphological changes, such as the transition from yeast to hyphae in Candida albicans during tissue invasion, affects recognition by CLRs and impacts on adaptive immune responses. CLRs recognize the fungal component of the microbiome that can influence T cell responses during infection at intestinal and peripheral sites.