6 results match your criteria: "and Infectious and Immunologic Diseases Research Center (IIDRC)[Affiliation]"
The autoimmune signature of hyperinflammatory multisystem inflammatory syndrome in children.
J Clin Invest
October 2021
Departments of Pediatrics, Division of Infectious Diseases and Immunology, and Infectious and Immunologic Diseases Research Center (IIDRC), Department of Biomedical Sciences and.
Multisystem inflammatory syndrome in children (MIS-C) manifests as a severe and uncontrolled inflammatory response with multiorgan involvement, occurring weeks after SARS-CoV-2 infection. Here, we utilized proteomics, RNA sequencing, autoantibody arrays, and B cell receptor (BCR) repertoire analysis to characterize MIS-C immunopathogenesis and identify factors contributing to severe manifestations and intensive care unit admission. Inflammation markers, humoral immune responses, neutrophil activation, and complement and coagulation pathways were highly enriched in MIS-C patient serum, with a more hyperinflammatory profile in severe than in mild MIS-C cases.
View Article and Find Full Text PDFSeroprevalence of antibodies to SARS-CoV-2 in healthcare workers: a cross-sectional study.
BMJ Open
February 2021
Department of Cardiology, Cedars-Sinai Medical Center, Los Angeles, California, USA
Objective: We sought to determine the extent of SARS-CoV-2 seroprevalence and the factors associated with seroprevalence across a diverse cohort of healthcare workers.
Design: Observational cohort study of healthcare workers, including SARS-CoV-2 serology testing and participant questionnaires.
Settings: A multisite healthcare delivery system located in Los Angeles County.
Kawasaki disease: pathophysiology and insights from mouse models.
Nat Rev Rheumatol
July 2020
Departments of Pediatrics, Division of Infectious Diseases and Immunology, and Infectious and Immunologic Diseases Research Center (IIDRC), Department of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
Kawasaki disease is an acute febrile illness and systemic vasculitis of unknown aetiology that predominantly afflicts young children, causes coronary artery aneurysms and can result in long-term cardiovascular sequelae. Kawasaki disease is the leading cause of acquired heart disease among children in the USA. Coronary artery aneurysms develop in some untreated children with Kawasaki disease, leading to ischaemic heart disease and myocardial infarction.
View Article and Find Full Text PDFPlatelets Fuel the Inflammasome Activation of Innate Immune Cells.
Cell Rep
May 2020
Institute of Innate Immunity, Medical Faculty, University of Bonn, 53127 Bonn, NRW, Germany. Electronic address:
The inflammasomes control the bioactivity of pro-inflammatory cytokines of the interleukin (IL)-1 family. The inflammasome assembled by NLRP3 has been predominantly studied in homogeneous cell populations in vitro, neglecting the influence of cellular interactions that occur in vivo. Here, we show that platelets boost the inflammasome capacity of human macrophages and neutrophils and are critical for IL-1 production by monocytes.
View Article and Find Full Text PDFChlamydia pneumoniae Hijacks a Host Autoregulatory IL-1β Loop to Drive Foam Cell Formation and Accelerate Atherosclerosis.
Cell Metab
September 2018
Departments of Pediatrics and Medicine, Division of Infectious Diseases and Immunology, and Infectious and Immunologic Diseases Research Center (IIDRC), Department of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA; David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Article Synopsis
- Chlamydia pneumoniae (C.pn) infection increases inflammation and accelerates atherosclerosis by activating the NLRP3 inflammasome, especially in hyperlipidemic conditions.
- C.pn infection enhances the activity of inflammatory processes in macrophages and foam cells, which are key players in atherosclerotic lesions, through the secretion of extracellular IL-1β.
- The study suggests that C.pn disrupts cholesterol export from macrophages by interfering with the function of the ABCA1 transporter, indicating potential therapeutic avenues using NLRP3 inhibitors to reduce atherosclerosis risk.
Ogg1-Dependent DNA Repair Regulates NLRP3 Inflammasome and Prevents Atherosclerosis.
Circ Res
September 2016
From the Departments of Pediatrics, Biomedical Sciences, and Infectious and Immunologic Diseases Research Center (IIDRC) (G.T., K.S., J.D., T.R.C., W.Z., S.C.), Department of Pathology (D.L.), Cedars-Sinai Medical Center, Los Angeles, CA; Department of Medicine, Barbra Streisand Women's Heart Center, Heart Institute of Cedars-Sinai (R.A.G.), Cedars-Sinai Medical Center, Los Angeles, CA; and David Geffen School of Medicine, University of California, Los Angeles (M.A.).
Rationale: Activation of NLRP3 (nucleotide-binding domain and leucine-rich repeat pyrin domain containing 3) inflammasome-mediating interleukin (IL)-1β secretion has emerged as an important component of inflammatory processes in atherosclerosis. Mitochondrial DNA (mtDNA) damage is detrimental in atherosclerosis, and mitochondria are central regulators of the nucleotide-binding domain and leucine-rich repeat pyrin domain containing 3 inflammasome. Human atherosclerotic plaques express increased mtDNA damage.
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