Fungal infections (mycoses) linked to at least six classes of fungus(Candida, Aspergillus, etc.) mainly cause infections of the skin and respiratory tract. Invasive infections observed in fragile subjects are relatively frequent and often fatal. A distinction is made between endemic mycoses and opportunistic mycoses observed only in immunocompromised subjects. Some fungi, such as Candida, are commensals. It is essential to understand the mechanisms that distinguish colonization of certain epithelial surfaces, such as the skin, from mucocutaneous infection and invasion (crossing the epithelial barrier). They involve the local microbial ecology and the degree of involvement of innate and adaptive immune responses. All innate immune cells can be activated by the recognition of polysaccharides present in the fungal wall. Numerous receptors are involved, inducing the production of pro-inflammatory cytokines and the activation of phagocytic cells to kill fungi by several mechanisms. One interesting aspect is that macrophagic cells retain a heightened response capacity after fungal infection, making them more effective at controlling the infection. This is known as " trained immunity ". Activation of innate immunity coordinates the differentiation of CD4 T lymphocytes into so-called "TH17" effector cells, which attract polynuclear cells to the site of infection via cytokine production, and activate epithelial cells to defend themselves. The molecular determinism of this response is now well understood. Control of a systemic (invasive) fungal infection depends essentially on the involvement of phagocytic cells - neutrophils and macrophages.
15:00 - 16:30
