Ligand binding to extracellular Toll-like receptors (TLRs), such as TLR2 and TLR4, leads to the production of pro-inflammatory cytokines during Candida infections. Finally, we explain the consequences of the Candida–host immune system interaction and discuss the future challenges for the field. Most studies to date have investigated host defences against Candida albicans, which is the most abundant Candida species in humans for this reason, we focus on C. In addition, we discuss the emerging data suggesting that the host may develop innate (or 'trained') memory in addition to the well-known adaptive memory responses to Candida species. We describe the various pattern recognition receptors (PRRs) that are involved in sensing Candida species and explain how both innate and adaptive immune cells, as well as non-immune cells, contribute to the antifungal response. In this Review, we provide a detailed account of the interaction of Candida species with the immune system. In patients with invasive candidiasis, treatment with antifungal drugs has shown only partial success in improving prognosis, and it is believed that only adjunctive immunotherapy could further improve the outcome of these infections. However, they can cause severe invasive disease when tissue homeostasis is disrupted - for example, in patients with neutropenia, pancreatitis or renal insufficiency - or following treatment with glucocorticosteroids, systemic antibiotics, indwelling medical devices, total parenteral nutrition or major abdominal surgery 1, 2, 3. In healthy individuals, Candida species are commensal in nature and colonize mucous membranes and the skin 1. ![]() Systems biology approaches combining innovative genomic, microbiome and functional data open new possibilities for identifying key mechanisms in the pathophysiology of fungal infections.įuture efforts need to combine cutting-edge molecular and cell-biological techniques with translational approaches in order to gain a better understanding of the host immune response to Candida infections and enable the design of novel antifungal strategies.Ĭandida species are fungi that have a major role in human pathology. ![]() albicans and components from its cell wall, particularly β-glucans, have the capacity to induce epigenetic reprogramming of innate immune cells, generating a de facto innate immune memory that has been termed 'trained immunity'. Neutrophils, monocytes and macrophages are the main immune cell populations responsible for host defence against systemic candidiasis, whereas T helper 1 (T H1) cells, T H17 cells and innate lymphoid cells are mainly responsible for protection against Candida infections at mucosal surfaces.Ĭ. C-type lectin receptors (CLRs) are the main family of PRRs involved in recognition of Candida species, but Toll-like receptors, NOD-like receptors and RIG-I-like receptors are also involved in the antifungal response. ![]() Innate immune recognition by pattern recognition receptors (PRRs) is the first step for activation of host defence mechanisms during Candida infections. Candida albicans is the most important fungal pathogen in humans, and it causes both mucosal and systemic fungal infections.
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