Pro-inflammatory effects of interleukin-35 in rheumatoid arthritis

Kód výsledku v 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>

Nalezeny alternativní kódy

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

Výsledek na webu

<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>

Jazyk výsledku

angličtina

Název v původním jazyce

Pro-inflammatory effects of interleukin-35 in rheumatoid arthritis

Popis výsledku v původním jazyce

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.

Název v anglickém jazyce

Pro-inflammatory effects of interleukin-35 in rheumatoid arthritis

Popis výsledku anglicky

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.

Druh

J_x - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)

CEP obor

CE - Biochemie

OECD FORD obor

—

Projekt

<a href="/cs/project/NT12440" target="_blank" >NT12440: IL-35: nový cytokin v patogenezi systémových revmatických onemocnění</a><br>

Návaznosti

V - Vyzkumna aktivita podporovana z jinych verejnych zdroju

Rok uplatnění

2015

Kód důvěrnosti údajů

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

Název periodika

Cytokine

ISSN

1043-4666

e-ISSN

—

Svazek periodika

73

Číslo periodika v rámci svazku

1

Stát vydavatele periodika

GB - Spojené království Velké Británie a Severního Irska

Počet stran výsledku

8

Strana od-do

36-43

Kód UT WoS článku

000353078500006

EID výsledku v databázi Scopus

2-s2.0-84922988798