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    Felty's syndrome autoantibodies bind to deiminated histones and neutrophil extracellular chromatin traps.

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    Authors
    Dwivedi, Nishant
    Upadhyay, Jagriti
    Neeli, Indira
    Khan, Salar
    Pattanaik, Debendra
    Myers, Linda
    Kirou, Kyriakos A.
    Hellmich, Bernhard
    Knuckley, Bryan
    Thompson, Paul R
    Crow, Mary K.
    Mikuls, Ted R.
    Csernok, Elena
    Radic, Marko
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    UMass Chan Affiliations
    Department of Biochemistry and Molecular Pharmacology
    Document Type
    Journal Article
    Publication Date
    2012-04-01
    Keywords
    Adolescent
    Adult
    Aged
    Aged, 80 and over
    Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis
    Arthritis, Rheumatoid
    Autoantibodies
    Autoantigens
    Felty Syndrome
    Female
    Histones
    Humans
    Lupus Erythematosus, Systemic
    Male
    Middle Aged
    Neutrophils
    Biochemistry
    Enzymes and Coenzymes
    Medicinal-Pharmaceutical Chemistry
    Musculoskeletal Diseases
    Therapeutics
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    Link to Full Text
    http://dx.doi.org/10.1002/art.33432
    Abstract
    OBJECTIVE: To test the hypothesis that autoantigen modifications by peptidylarginine deiminase type 4 (PAD-4) increase immunoreactivity. METHODS: We assembled sera from patients with systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), Felty's syndrome (FS), and antineutrophil cytoplasmic antibody-associated vasculitides (AAVs), as well as sera from control subjects without autoimmune diseases. The sera were tested for binding to activated neutrophils, deiminated histones, and neutrophil extracellular chromatin traps (NETs). IgG binding to lipopolysaccharide-activated neutrophils was assessed with confocal microscopy, and binding to in vitro-deiminated histones was measured using enzyme-linked immunosorbent assay (ELISA) and Western blotting. In addition, we quantitated histone deimination in freshly isolated neutrophils from the blood of patients and control subjects. RESULTS: Increased IgG reactivity with activated neutrophils, particularly binding to NETs, was paralleled by preferential binding to deiminated histones over nondeiminated histones by ELISA in a majority of sera from FS patients but only in a minority of sera from SLE and RA patients. Immunoblotting revealed autoantibody preference for deiminated histones H3, H4, and H2A in most FS patients and in a subset of SLE and RA patients. In patients with AAVs, serum IgG preferentially bound nondeiminated histones over deiminated histones. Increased levels of deiminated histones were detected in neutrophils from RA patients. CONCLUSION: Circulating autoantibodies in FS are preferentially directed against PAD-4-deiminated histones and bind to activated neutrophils and NETs. Thus, increased reactivity with modified autoantigens in FS implies a direct contribution of neutrophil activation and the production of NET-associated nuclear autoantigens in the initiation or progression of FS.
    Source
    Arthritis Rheum. 2012 Apr;64(4):982-92. doi: 10.1002/art.33432. Epub 2011 Oct 27. Link to article on publisher's site
    DOI
    10.1002/art.33432
    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/50027
    Notes

    At the time of publication, Paul Thompson was not yet affiliated with UMass Medical School.

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    Link to Article in PubMed
    ae974a485f413a2113503eed53cd6c53
    10.1002/art.33432
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