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Chronic systemic inflammation (SI) is the result of release of pro-inflammatory cytokines from immune-related cells and the chronic activation of the innate immune system.It can contribute to the development or progression of certain conditions such as cardiovascular disease, cancer, diabetes mellitus, chronic kidney disease, non-alcoholic fatty liver disease, autoimmune and neurodegenerative ...
Inflammatory myopathy, also known as idiopathic inflammatory myopathy (IIM), is disease featuring muscle weakness, inflammation of muscles , and in some types, muscle pain . The cause of much inflammatory myopathy is unknown ( idiopathic ), and such cases are classified according to their symptoms and signs , electromyography , MRI , and ...
Due to its proinflammatory action, a proinflammatory cytokine tends to make the disease itself or the symptoms correlated to a disease worse by causing fever, inflammation, tissue destruction, and in some cases, even shock and death. [7] Excessive amounts of proinflammatory cytokines have been shown to cause detrimental effects [2]
Type 2 inflammation is a pattern of immune response. Its physiological function is to defend the body against helminths , but a dysregulation of the type 2 inflammatory response has been implicated in the pathophysiology of several diseases.
The regulation of DAMP signaling can be a potential therapeutic target to reduce inflammation and treat diseases. For example, administration of neutralizing HMGB1 antibodies or truncated HMGB1-derived A-box protein ameliorated arthritis in collagen-induced arthritis rodent models. Clinical trials with HSP inhibitors have also been reported.
The most predictive biomarkers 36h after CAR-T infusion of CRS are a fever ≥38.9 °C (102 °F) and elevated levels of MCP-1 in serum. [12] Many of the cytokines elevated in CRS are not produced by CAR-T cells, but by myeloid cells that are pathogenically licensed through T-cell-mediated activating mechanisms.
The inflammasome was discovered by the team of Jürg Tschopp, at the University of Lausanne, in 2002. [17] [18] In 2002, it was first reported by Martinon et al. [17] that NLRP1 (NLR family PYD-containing 1) could assemble and oligomerize into a structure in vitro, which activated the caspase-1 cascade, thereby leading to the production of pro-inflammatory cytokines, including IL-1β and IL-18.
TNF is believed to trigger cell death in inflammatory diseases due to elevated levels of interfering cytokines, elevated levels of TNFR2 signalling, or genetic mutations. Drugs that target proteins involved in TNF-induced cell death, such as RIPK1, are being evaluated for their efficacy against autoinflammatory diseases.