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• W2583839717 abstract "Fungi cause different disease types, from common superficial infections to invasive or deep-seated severe infections. Host defense mechanisms determine the clinical outcome of fungal infections, either being inadequate and failing to control infection, being too exuberant and contributing to tissue damage or failing to resolve properly leading to persistent inflammation and fibrosis. The recognition pathways of the innate immune systems, the phagocytes and other immune effector cells, cytokines and other molecules work together to control and contain fungal infections. Recently discovered intracellular receptors are the NLR- NLRP3 inflammasomes and Damage-associated molecular patterns (DAMPs). It has been shown of recent that Neutrophils extracellular traps (NETS) aid in the killing of fungi and Macrophage migration inhibition factor (MIF) plays a role in resistance to fungal infection. In the past, protective immunity to fungi has been known to be by Th- 1 response driven by the 1L-12-IFNγ axis. Recently, other pathways of cytokines and T-cells have been implicated in the immunity to fungal infections; these are Th-17 cells and IL-17, IL23, and IL22. Central to the formation of different T-cell subsets and cytokines, is the discovery that Dendritic cells exhibit plasticity on exposure to different forms of fungi, using different recognition receptors. Keywords - Cytokines,Fungi,Phagocytes,Toll-like receptors,T-Lymphocytes." @default.
• W2583839717 created "2017-02-10" @default.
• W2583839717 creator A5078048302 @default.
• W2583839717 date "2015-01-01" @default.
• W2583839717 modified "2023-09-26" @default.
• W2583839717 title "Host Protective Immunity to Fungal Infections-Recent Advances" @default.
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