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Pro-inflammatory effects of interleukin-35 in rheumatoid arthritis

机译：白细胞介素35在类风湿关节炎中的促炎作用

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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 (IL12Rβ2/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 TNFα in RASFs and PBMCs. IL-35 dose-dependently upregulated release of pro-inflammatory mediators IL-1β, 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 IL12Rβ2 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.
机译：目的：白介素35（IL-35）是IL-12家族的异二聚成员，由p35 / IL-12a和EBI3 / IL-27b亚基组成。 IL-35在鼠Treg细胞中表达，可控制小鼠模型中的炎症性疾病。然而，人IL-35在Teff细胞中而不是在Treg细胞中表达，并且在炎性条件下显示出上调。我们的目的是检查IL-35在类风湿关节炎（RA）的发病机理中的作用。方法：采用免疫组织化学和免疫荧光分析法测定RA，骨关节炎（OA）和银屑病关节炎（PsA）滑膜中IL-35及其亚基（p35 / EBI3）和IL-35受体（IL12Rβ2/ gp130）的表达和定位。组织。在RA滑膜成纤维细胞（SF）和外周血单核细胞（PBMC）中评估了IL-35刺激后p35 / EBI3亚基的表达和炎性细胞因子的释放。结果：与OA或PsA滑膜相比，RA中IL-35及其亚基均上调。使用细胞特异性标记，在RA滑膜的巨噬细胞，树突状细胞，SF和T以及B细胞中鉴定出p35和EBI3。 TNFα在RASF和PBMC中均诱导了p35和EBI3。 IL-35剂量依赖性上调PBMC中促炎性介质IL-1β，IL-6和MCP-1的释放。虽然gp130受体亚基在RA滑膜中上调并在RASF和PBMC中表达，但组织之间IL12Rβ2表达亚基没有差异，并且在RASF中缺乏它。结论：RA炎症部位IL-35的上调及其促炎潜力提示IL-35可能在RA发病中起重要作用。

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