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- W1569288456 abstract "The human body is constantly exposed to a variety of microbes and their metabolites. In order to prevent and eliminate the threat posed by the microbes, our body has evoked with a sophisticated defence system, which has two arms: innate and adaptive immunity. The innate immunity forms the first line of defence consisting of mechanical, chemical, and microbiological barriers. In addition, it contains different groups of immune cells and specialized proteins that are responsible for the rapid detection of a threat. In the early stage of an infection, the cells of innate immunity, including dendritic cells (DCs), macrophages, neutrophils and natural killer (NK) cells initiate a rapid immune response mediated via the different pattern recognition receptors (PRRs) expressed by these cells. PRRs, including membrane-bound Tolllike receptors (TLRs), C-type lectin -like receptors (CLRs), and cytoplasmic NODlike receptors (NLRs) recognize different pathogen associated molecular patterns (PAMPs) produced by the microbes. In addition to PAMPs, particular NLRs are able to sense several danger associated molecular patterns (DAMPs) of both endogenous and exogenous origins. Efficient PRR mediated PAMP and DAMP detection leads to the immune response ultimately resulting in the eradication of the pathogen by the combined actions of innate and adaptive immune systems. Activation of PRRs with PAMPs and DAMPs leads to expression of various cytokines such as pro-inflammatory cytokines interleukin-1β (IL-1β) and IL-18 in immune cells. The secretion of pyrogenic IL-1β is normally strictly silenced. In contrast to IL-1β, IL-18 is basally expressed although its production is controlled at several levels by immune cells. NLR containing multiprotein complexes called inflammasomes are considered as key mediators of inflammation. Inflammasome mediated signalling is needed for the processing of immature pro-IL-1β into its biologically active IL-1β form, which is then secreted. More specifically, the pro-IL1β is cleaved by cysteine protease caspase-1, which in turn needs to be activated by the inflammasome. In general, separate signals are needed for the activation of IL-1β mRNA expression and pro-IL-1β production and further for the processing of proIL-1β and IL-1β secretion. In parallel, pro-IL-18 requires inflammasome associated caspase-1 mediated processing before it attains its biological activity. Human beings are constantly encountering fungi and their metabolic products, which are sensed through different PPRs expressed by immune cells. This thesis revealed that a major fungal cell wall component, (1,3)-β-glucans, triggers secretion of IL-1β in human macrophages. First, (1,3)-β-glucan triggered the activation of dectin-1, a receptor belonging to CLR family, which resulted in the transcriptional induction of IL-1β and the production of pro-IL-1β. Secondly, the dectin-1 signalling activated" @default.
- W1569288456 created "2016-06-24" @default.
- W1569288456 creator A5073058257 @default.
- W1569288456 date "2014-05-23" @default.
- W1569288456 modified "2023-09-25" @default.
- W1569288456 title "Activation of the inflammasome by (1,3)-β-glucans and trichothecene mycotoxins in human macrophages" @default.
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