A fecal bacterial strain cross-reacts with rheumatoid arthritis autoantibodies, stimulates CD4 T cells, and induces joint disease in mice.
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Hunting the origin and source of NR1-directed IgGs in patients with encephalitis.
Brain Behav Immun
August 2024
Oxford Autoimmune Neurology Group, Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, UK; Departments of Neurology and Neurosciences, Mayo Clinic, Jacksonville, FL, USA. Electronic address:
Proteinase 3 promotes formation of multinucleated giant cells and granuloma-like structures in patients with granulomatosis with polyangiitis.
Ann Rheum Dis
June 2023
UCL Department of Renal Medicine, Royal Free Hospital, London, UK
Objectives: Granulomatosis with polyangiitis (GPA) and microscopic polyangiitis (MPA) are autoimmune vasculitides associated with antineutrophil cytoplasm antibodies that target proteinase 3 (PR3) or myeloperoxidase (MPO) found within neutrophils and monocytes. Granulomas are exclusively found in GPA and form around multinucleated giant cells (MGCs), at sites of microabscesses, containing apoptotic and necrotic neutrophils. Since patients with GPA have augmented neutrophil PR3 expression, and PR3-expressing apoptotic cells frustrate macrophage phagocytosis and cellular clearance, we investigated the role of PR3 in stimulating giant cell and granuloma formation.
View Article and Find Full Text PDFFishing with autoantibodies nets a gut bacteria that drives arthritis.
Sci Immunol
December 2022
Department of Dermatology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA; email:
A fecal bacterial strain cross-reacts with rheumatoid arthritis autoantibodies, stimulates CD4 T cells, and induces joint disease in mice.
View Article and Find Full Text PDFGlomerular Endothelial Cell-Derived microRNA-192 Regulates Nephronectin Expression in Idiopathic Membranous Glomerulonephritis.
J Am Soc Nephrol
November 2021
Department of Nephrology, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen, Germany.
Background: Autoantibodies binding to podocyte antigens cause idiopathic membranous glomerulonephritis (iMGN). However, it remains elusive how autoantibodies reach the subepithelial space because the glomerular filtration barrier (GFB) is size selective and almost impermeable for antibodies.
Methods: Kidney biopsies from patients with iMGN, cell culture, zebrafish, and mouse models were used to investigate the role of nephronectin (NPNT) regulating microRNAs (miRs) for the GFB.
Glycine Receptor Autoantibodies Impair Receptor Function and Induce Motor Dysfunction.
Ann Neurol
September 2020
Institute for Clinical Neurobiology, University Hospital, Julius Maximilian University of Würzburg, Würzburg, Germany.
Objective: Impairment of glycinergic neurotransmission leads to complex movement and behavioral disorders. Patients harboring glycine receptor autoantibodies suffer from stiff-person syndrome or its severe variant progressive encephalomyelitis with rigidity and myoclonus. Enhanced receptor internalization was proposed as the common molecular mechanism upon autoantibody binding.
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