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    Synovial fibroblast-neutrophil interactions promote pathogenic adaptive immunity in rheumatoid arthritis

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    Authors
    Carmona-Rivera, Carmelo
    Thompson, Paul R
    Kaplan, Mariana J.
    UMass Chan Affiliations
    Thompson Lab
    Department of Biochemistry and Molecular Pharmacology
    Document Type
    Journal Article
    Publication Date
    2017-04-14
    Keywords
    Biochemistry
    Immunology and Infectious Disease
    Immunopathology
    Rheumatology
    
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    Link to Full Text
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5479641/
    Abstract
    Rheumatoid arthritis (RA) is characterized by synovial joint inflammation and by development of pathogenic humoral and cellular autoimmunity to citrullinated proteins. Neutrophil extracellular traps (NETs) are a source of citrullinated autoantigens and activate RA synovial fibroblasts (FLS), cells crucial in joint damage. We investigated the molecular mechanisms by which NETs promote proinflammatory phenotypes in FLS, and whether these interactions generate pathogenic anti-citrulline adaptive immune responses. NETs containing citrullinated peptides are internalized by FLS through a RAGE-TLR9 pathway promoting FLS inflammatory phenotype and their upregulation of MHC class II. Once internalized, arthritogenic NET-peptides are loaded into FLS MHC class II and presented to Ag-specific T cells. HLADRB1*0401 transgenic mice immunized with mouse FLS loaded with NETs develop antibodies specific to citrullinated forms of relevant RA autoantigens implicated in RA pathogenesis as well as cartilage damage. These results implicate FLS as mediators in RA pathogenesis, through the internalization and presentation of NET citrullinated peptides to the adaptive immune system leading to pathogenic autoimmunity and cartilage damage.
    Source
    Sci Immunol. 2017 Apr;2(10). pii: eaag3358. doi: 10.1126/sciimmunol.aag3358. Epub 2017 Apr 14. Link to article on publisher's site
    DOI
    10.1126/sciimmunol.aag3358
    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/40344
    PubMed ID
    28649674
    Notes

    Full list of authors omitted for brevity. For full list see article.

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    Link to Article in PubMed

    ae974a485f413a2113503eed53cd6c53
    10.1126/sciimmunol.aag3358
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