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    Immune checkpoint inhibitor PD-1 pathway is down-regulated in synovium at various stages of rheumatoid arthritis disease progression.

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    Authors
    Guo, Yanxia
    Walsh, Alice M
    Canavan, Mary
    Wechalekar, Mihir D
    Cole, Suzanne
    Yin, Xuefeng
    Scott, Brittney
    Loza, Mathew
    Orr, Carl
    McGarry, Trudy
    Bombardieri, Michele
    Humby, Frances
    Proudman, Susanna M
    Pitzalis, Costantino
    Smith, Malcolm D
    Friedman, Joshua R
    Anderson, Ian
    Madakamutil, Loui
    Veale, Douglas J
    Fearon, Ursula
    Nagpal, Sunil
    Show allShow less
    Issue Date
    2018
    MeSH
    Arthritis, Rheumatoid
    Disease Progression
    Down-Regulation
    Female
    Humans
    Male
    Programmed Cell Death 1 Receptor
    Synovial Membrane
    
    Metadata
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    Citation
    Immune checkpoint inhibitor PD-1 pathway is down-regulated in synovium at various stages of rheumatoid arthritis disease progression. 2018, 13 (2):e0192704 PLoS ONE
    Publisher
    PLoS One
    Journal
    PloS one
    URI
    http://hdl.handle.net/10147/622950
    DOI
    10.1371/journal.pone.0192704
    PubMed ID
    29489833
    Additional Links
    http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0192704
    Abstract
    Immune checkpoint blockade with therapeutic anti-cytotoxic T lymphocyte-associated antigen (CTLA)-4 (Ipilimumab) and anti-programmed death (PD)-1 (Nivolumab and Pembrolizumab) antibodies alone or in combination has shown remarkable efficacy in multiple cancer types, concomitant with immune-related adverse events, including arthralgia and inflammatory arthritis (IA) in some patients. Herein, using Nivolumab (anti-PD-1 antagonist)-responsive genes along with transcriptomics of synovial tissue from multiple stages of rheumatoid arthritis (RA) disease progression, we have interrogated the activity status of PD-1 pathway during RA development. We demonstrate that the expression of PD-1 was increased in early and established RA synovial tissue compared to normal and OA synovium, whereas that of its ligands, programmed death ligand-1 (PD-L1) and PD-L2, was increased at all the stages of RA disease progression, namely arthralgia, IA/undifferentiated arthritis, early RA and established RA. Further, we show that RA patients expressed PD-1 on a majority of synovial tissue infiltrating CD4+ and CD8+ T cells. Moreover, enrichment of Nivolumab gene signature was observed in IA and RA, indicating that the PD-1 pathway was downregulated during RA disease progression. Furthermore, serum soluble (s) PD-1 levels were increased in autoantibody positive early RA patients. Interestingly, most of the early RA synovium tissue sections showed negative PD-L1 staining by immunohistochemistry. Therefore, downregulation in PD-1 inhibitory signaling in RA could be attributed to increased serum sPD-1 and decreased synovial tissue PD-L1 levels. Taken together, these data suggest that agonistic PD1 antibody-based therapeutics may show efficacy in RA treatment and interception.
    Item Type
    Article
    Language
    en
    ISSN
    1932-6203
    ae974a485f413a2113503eed53cd6c53
    10.1371/journal.pone.0192704
    Scopus Count
    Collections
    St. Vincent's University Hospital

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