Topic: caspase-1

Recently found association linking viral infections to neurodegenerative diseases has raised concerns about unknown mechanisms in the communication between the respiratory and central nervous systems . We hypothesized that extracellular vesicles (EVs) can transfer viral signals to microglia, triggering the upregulation of pro-inflammatory cytokines by activating inflammasome-related pathways. In this study, we investigate the role of EVs released from virus mimetic poly I:C-infected human airway epithelial cells in modulating microglial immune responses. EVs were isolated from poly I:C-primed

Relapsing remitting multiple sclerosis (RRMS) hits around 85% MS patients. The main disease modifying therapies (DMTs) of this subtype are: Fingolimod (Gilenya), IFN-β A1(Rebif & Avonex), Teriflunomide(Aubagio), IFN-β 1B(β-feron) and Dimethyl Fumarate(Marovarex).The study aimed at: 1.Expression profiling of long non-coding RNA MALAT-1 in RRMS patients, MALAT1 knockdown and evaluating successful silencing of MALAT1 by specific siRNAs, 2.Expression profiling of Inflammasome components in RRMS patients and studying the impact of MALAT1-knock down on them, 3.Expression profiling of Calreticuli

Type I interferon (IFN-I) is a pivotal cytokine of the innate immune response, playing a significant role in the pathophysiology of inflammation-induced damage in the central nervous system (CNS). Enhanced, constitutive IFN-I signaling is a defining feature of a number of Mendelian inborn errors of immunity, which are coined type I interferonopathies. However, understanding the pathophysiology of these disorders is hindered by the inability of numerous animal models to replicate the neurological phenotype essential for these diseases. Fortunately, we have recently generated and characterized t