Arthritis in systemic lupus erythematosus is characterized by local IL-17A and IL-6 expression in synovial fluid.
Arthritis in systemic lupus erythematosus is characterized by local IL-17A and IL-6 expression in synovial fluid.
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DOI：
10.1111/cei.13585
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发表时间：
2021-07
影响因子：
4.6
通讯作者：
Malmström V
中科院分区：
文献类型：
--
作者：
Sippl N;Faustini F;Rönnelid J;Turcinov S;Chemin K;Gunnarsson I;Malmström V
关节炎是系统性红斑狼疮（SLE）的常见临床特征，通常为非糜烂性，与类风湿性关节炎（RA）相反。虽然类风湿关节炎的滑膜病理学已被广泛研究，但对狼疮性关节炎的病理生理学知之甚少。在这里，我们的目的是探讨关节炎表现的SLE患者滑液中的细胞因子和细胞成分。使用细胞因子微珠阵列分析SLE患者（n = 17）的无细胞滑液和配对血清样本中的T辅助细胞相关细胞因子。从2例SLE患者的滑膜液中采集单个核细胞（SFMC），采用多参数流式细胞术分析其T细胞、B细胞、单核细胞和树突状细胞表型。在体外进一步刺激SLE衍生的SFMC以测量其产生干扰素（IFN）-γ和白细胞介素（IL）-17A的能力。所有患者均符合ACR 1982 SLE分类标准。对临床记录进行了审查，以排除合并症的存在，如骨关节炎或与RA重叠。SLE滑液中IL-17 A和IL-6水平较高。一个明确的滑膜CD 4 + T细胞亚群表达CCR 6+，这是一种与辅助性T细胞17型（Th 17）相关的标志物。体外刺激后，在CD 4 + CCR 6 + T细胞中验证了IL-17 A-的产生。此外，在CD 4+和CD 8+细胞中均观察到强烈的IFN-γ产生。我们的研究显示狼疮性关节炎患者滑液中IL-17 A和IL-6水平较高。Th 17通路与SLE疾病发病机制的几个方面有关，我们的数据也表明Th 17参与了狼疮关节炎。SLE关节炎患者滑液中IL-17 A和IL-6升高。Th 17通路与SLE疾病发病机制的几个方面有关，我们的数据表明Th 17也参与了狼疮关节炎。
Arthritis is a common clinical feature of systemic lupus erythematosus (SLE) and is usually non‐erosive, as opposed to rheumatoid arthritis (RA). While RA synovial pathology has been extensively studied, little is known about the pathophysiology of lupus arthritis. Here, we aimed to explore the cytokine and cellular compartments in synovial fluids of SLE patients with arthritic manifestations. Acellular synovial fluid and paired serum samples from SLE patients (n = 17) were analyzed with cytokine bead array for T helper‐associated cytokines. From two SLE patients, synovial fluid mononuclear cells (SFMC) could also be captured and were analyzed by multiparameter flow cytometry to dissect T cell, B cell, monocyte and dendritic cell phenotypes. SLE‐derived SFMC were further stimulated in vitro to measure their capacity for producing interferon (IFN)‐γ and interleukin (IL)‐17A. All patients fulfilled the ACR 1982 classification criteria for SLE. Clinical records were reviewed to exclude the presence of co‐morbidities such as osteoarthritis or overlap with RA. IL‐17A and IL‐6 levels were high in SLE synovial fluid. A clear subset of the synovial CD4+ T cells expressed CCR6+, a marker associated with T helper type 17 (Th17) cells. IL‐17A‐production was validated among CD4+CCR6+ T cells following in‐vitro stimulation. Furthermore, a strong IFN‐γ production was observed in both CD4+ and CD8+ cells. Our study shows high IL‐17A and IL‐6 levels in synovial fluids of patients with lupus arthritis. The Th17 pathway has been implicated in several aspects of SLE disease pathogenesis and our data also point to Th17 involvement for lupus arthritis. IL‐17A and IL‐6 are elevated in synovial fluid of SLE arthritis patients. The Th17 pathway have been implicated in several aspects of SLE disease pathogenesis and our data points to Th17 involvement also for lupus arthritis.
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影响因子：
--
作者：
Petri, Michelle;Orbai, Ana-Maria;Alarcon, Graciela S.;Gordon, Caroline;Merrill, Joan T.;Fortin, Paul R.;Bruce, Ian N.;Isenberg, David;Wallace, Daniel J.;Nived, Ola;Sturfelt, Gunnar;Ramsey-Goldman, Rosalind;Bae, Sang-Cheol;Hanly, John G.;Sanchez-Guerrero, Jorge;Clarke, Ann;Aranow, Cynthia;Manzi, Susan;Urowitz, Murray;Gladman, Dafna;Kalunian, Kenneth;Costner, Melissa;Werth, Victoria P.;Zoma, Asad;Bernatsky, Sasha;Ruiz-Irastorza, Guillermo;Khamashta, Munther A.;Jacobsen, Soren;Buyon, Jill P.;Maddison, Peter;Dooley, Mary Anne;van vollenhoven, Ronald F.;Ginzler, Ellen;Stoll, Thomas;Peschken, Christine;Jorizzo, Joseph L.;Callen, Jeffrey P.;Lim, S. Sam;Fessler, Barri J.;Inanc, Murat;Kamen, Diane L.;Rahman, Anisur;Steinsson, Kristjan;Franks, Andrew G., Jr.;Sigler, Lisa;Hameed, Suhail;Fang, Hong;Ngoc Pham;Brey, Robin;Weisman, Michael H.;McGwin, Gerald, Jr.;Magder, Laurence S.
通讯作者：
Magder, Laurence S.
影响因子：
2.6
作者：
Ball, E. M. A.;Gibson, D. S.;Rooney, M. R.
通讯作者：
Rooney, M. R.
DOI：
10.4049/jimmunol.1002653
发表时间：
2011-02-15
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Bowness P;Ridley A;Shaw J;Chan AT;Wong-Baeza I;Fleming M;Cummings F;McMichael A;Kollnberger S
通讯作者：
Kollnberger S
影响因子：
8
作者：
Bocharnikov, Alexandra, V;Keegan, Joshua;Rao, Deepak A.
通讯作者：
Rao, Deepak A.
影响因子：
39.2
作者：
LABOWITZ, R;SCHUMACH.R
通讯作者：
SCHUMACH.R