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Pro-inflammatory effects of interleukin-35 in rheumatoid arthritis

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11120%2F15%3A43909682" target="_blank" >RIV/00216208:11120/15:43909682 - isvavai.cz</a>

  • Alternative codes found

    RIV/00216208:11110/15:10294476 RIV/00064203:_____/15:10294476 RIV/00023728:_____/15:#0005062

  • Result on the web

    <a href="http://dx.doi.org/10.1016/j.cyto.2015.01.019" target="_blank" >http://dx.doi.org/10.1016/j.cyto.2015.01.019</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1016/j.cyto.2015.01.019" target="_blank" >10.1016/j.cyto.2015.01.019</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    Pro-inflammatory effects of interleukin-35 in rheumatoid arthritis

  • Original language description

    Objective: Interleukin-35 (IL-35) is a heterodimeric member of the IL-12 family consisting of p35/IL-12a and EBI3/IL-27b subunits. Expressed in murine Treg cells, IL-35 controls inflammatory diseases in mouse models. However, human IL-35 is expressed in Teff cells rather than in Treg cells and is shown to be upregulated under inflammatory conditions. Our aim was to examine the involvement of IL-35 in the pathogenesis of rheumatoid arthritis (RA). Methods: Immunohistochemical and immunofluorescence analysis was used to determine the expression and localization of IL-35 and its subunits (p35/EBI3) and IL-35 receptor (IL12R beta 2/gp130) in RA, osteoarthritis (OA) and psoriatic arthritis (PsA) synovial tissues. Expression of p35/EBI3 subunits and release of inflammatory cytokines upon stimulation with IL-35 were assessed in RA synovial fibroblasts (SFs) and peripheral blood mononuclear cells (PBMCs). Results: Both IL-35 and its subunits were upregulated in RA in comparison with OA or PsA synovium. Using cell-specific markers, p35 and EBI3 were identified in macrophages, dendritic cells, SFs, and T as well as B cells in RA synovium. Both p35 and EBI3 were induced by TNF alpha, in RASFs and PBMCs. IL-35 dose-dependently upregulated release of pro-inflammatory mediators IL-1 beta, IL-6 and MCP-1 in PBMCs. While gp130 receptor subunit was upregulated in RA synovium and was expressed in RASFs and PBMCs, there was no difference in IL12R beta 2 expression subunit among tissues and its presence in RASFs was lacking. Conclusion: Upregulation of IL-35 at sites of inflammation in RA and its pro-inflammatory potential suggests that IL-35 might play an important role in RA pathogenesis.

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>x</sub> - Unclassified - Peer-reviewed scientific article (Jimp, Jsc and Jost)

  • CEP classification

    CE - Biochemistry

  • OECD FORD branch

Result continuities

  • Project

    <a href="/en/project/NT12440" target="_blank" >NT12440: IL-35: a novel cytokine in systemic rheumatic diseases</a><br>

  • Continuities

    V - Vyzkumna aktivita podporovana z jinych verejnych zdroju

Others

  • Publication year

    2015

  • Confidentiality

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Data specific for result type

  • Name of the periodical

    Cytokine

  • ISSN

    1043-4666

  • e-ISSN

  • Volume of the periodical

    73

  • Issue of the periodical within the volume

    1

  • Country of publishing house

    GB - UNITED KINGDOM

  • Number of pages

    8

  • Pages from-to

    36-43

  • UT code for WoS article

    000353078500006

  • EID of the result in the Scopus database

    2-s2.0-84922988798