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    Home > Active Ingredient News > Blood System > Blood: IL-18 and cytotoxic damage are the independent and synergistic drivers of viral induced super-inflammation

    Blood: IL-18 and cytotoxic damage are the independent and synergistic drivers of viral induced super-inflammation

    • Last Update: 2020-07-13
    • Source: Internet
    • Author: User
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    Blood-phytomotic lymphocytic hyperactivity (HLH) and macrophage activation syndrome (MAS) are life-threatening hyper-inflammatory syndromes, usually associated with underlying blood disease and rheumatism, respectivelyFamilial HLH is associated with hertotoxicity damage and too much antigen presentationobserved extremely elevated serum leukocyte interleukin (IL)-18 in MAS patients, making it a potential target for MAS treatment, how IL-18 promotes super-inflammation remains unknownin adjwistic-induced MAS models, excess IL-18 can promoteimmuno
    pathology, but perforated deficiency has no effectTo determine the effect of excess IL-18 on viral-induced immunopathology, Paul Tsoukas et alinfected Il18 genetically modified (Il18tg) mice with the lymphocytic vasculature meningitis virus (LCMV, Armstrong)in wild (WT) mice, LCMV infection is self-limiting (self-healing), but in-/-mice, Prf1 can manifest as chronic viral emis and the deadly HLHThe Il18-gmogeneticd mice infected with LCMV developed a disease and super-inflammation, similar to Prf1-/-mice, although the mortality rate was lowerLike Prf1-/-
    mice, CD8 depletion or interferon-gamma (IFNg) blocking largely saved immunopathology; unlike Prf1-/-
    mice, Il18tg mice had normal target cell lethality and viral RNA/antigen removalexcess IL-8 acts on T lymphocytes to amplify their inflammatory reactions, rather than harming cytotoxicitySurprisingly, perforated deficiency combined with the generation of genetically modified IL-8 can trigger spontaneous super-inflammation characterized by CD8 T cell amplification, which IFNg blocking can improve this responseEven Il18tg;prf1-monoploid mice exhibited super inflammatory characteristics, excess IL-18 promotes super-inflammation through an autotoxic damage-different autotoxic ity and its own inflammatory mechanismData from this study show that IL-18 is a potential, independent, changeable driver of deadly congenital adaptive super-inflammation, supporting the fundamental principle of an IL-18-driven super-inflammatory subcategory
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