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可溶性肿瘤坏死因子样凋亡弱诱导剂和白细胞介素-17A在乳糜泻发病机制中的作用:一项横断面研究。

The role of soluble tumor necrosis factor like weak inducer of apoptosis and interleukin-17A in the etiopathogenesis of celiac disease: A cross-sectional study.

作者信息

Yuksel Mahmut, Kaplan Mustafa, Ates Ihsan, Kilic Zeki Mesut Yaln, Kilic Hasan, Suna Nuretdin, Ates Hale, Kayacetin Ertugrul

机构信息

aTurkey Yuksek Ihtisas Training and Research Hospital, Department of Gastroenterology bAnkara Numune Training and Research Hospital, Department of Internal Medicine cTurkey Yuksek Ihtisas Training and Research Hospital, Department of Microbiology dAtatürk Chest Diseases & Thoracic Surgery Training and Research Hospital, Department of Immunology and Allergy, Ankara, Turkey.

出版信息

Medicine (Baltimore). 2016 Jun;95(26):e3937. doi: 10.1097/MD.0000000000003937.

DOI:10.1097/MD.0000000000003937
PMID:27367991
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4937905/
Abstract

Our aim in this study was to determine soluble tumor necrosis factor (TNF)-like weak inducer of apoptosis (sTWEAK) and interleukin-17A (IL-17A) levels in celiac disease, and their association with the gluten diet and autoantibodies. Eighty patients with celiac diagnosis and 80 healthy control individuals with similar age, gender and body mass index to the patient group were included in the study. Serum sTWEAK and IL-17A levels were measured by the serum enzyme-linked immunosorbent assay kit. The median IL-17A (117.5 pg/mL vs. 56.7 pg/mL; P = 0.001) level in celiac patients was higher than in the control group, while the median sTWEAK (543 pg/mL vs. 643 pg/mL; P = 0.016) level in patients was determined to be lower. In the patient group, patients who complied with the gluten diet had a lower level of median IL-17A (98.1 pg/mL vs. 197.5 pg/mL; P = 0.034) and a higher level of sTWEAK (606 pg/mL vs. 522.8 pg/mL; P = 0.031) than those who did not adhere. Furthermore, the IL-17A level was higher and the sTWEAK level was lower in celiac patients with positive antibody than those with negative antibody. A positive correlation was determined among anti-gliadin antibody IgA, anti-gliadin antibody IgG, anti-tissue transglutaminase IgG levels and the IL-17A level, and a negative correlation was determined with the sTWEAK level. In celiac disease, the sTWEAK and IL-17A levels differ between patients who cannot adapt to the gluten diet and who are autoantibody positive, and patients who adapt to the diet and are autoantibody negative. We believe that sTWEAK and IL-17A are associated with the inflammation in celiac pathogenesis.

摘要

本研究的目的是测定乳糜泻患者中可溶性肿瘤坏死因子(TNF)样凋亡弱诱导因子(sTWEAK)和白细胞介素-17A(IL-17A)的水平,以及它们与麸质饮食和自身抗体的关联。本研究纳入了80例确诊为乳糜泻的患者以及80名年龄、性别和体重指数与患者组相似的健康对照个体。采用血清酶联免疫吸附测定试剂盒检测血清sTWEAK和IL-17A水平。乳糜泻患者的IL-17A中位数水平(117.5 pg/mL对56.7 pg/mL;P = 0.001)高于对照组,而患者的sTWEAK中位数水平(543 pg/mL对643 pg/mL;P = 0.016)则较低。在患者组中,遵循麸质饮食的患者IL-17A中位数水平(98.1 pg/mL对197.5 pg/mL;P = 0.034)较低,而sTWEAK水平(606 pg/mL对522.8 pg/mL;P = 0.031)较高。此外,抗体阳性的乳糜泻患者的IL-17A水平较高,而sTWEAK水平较低。抗麦醇溶蛋白抗体IgA、抗麦醇溶蛋白抗体IgG、抗组织转谷氨酰胺酶IgG水平与IL-17A水平呈正相关,与sTWEAK水平呈负相关。在乳糜泻中,无法适应麸质饮食且自身抗体阳性的患者与适应饮食且自身抗体阴性的患者之间,sTWEAK和IL-17A水平存在差异。我们认为sTWEAK和IL-17A与乳糜泻发病机制中的炎症有关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f03/4937905/f8b77c7332e0/medi-95-e3937-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f03/4937905/f8b77c7332e0/medi-95-e3937-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f03/4937905/f8b77c7332e0/medi-95-e3937-g002.jpg

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本文引用的文献

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Th17, intestinal microbiota and the abnormal immune response in the pathogenesis of celiac disease.Th17、肠道微生物群与乳糜泻发病机制中的异常免疫反应。
Gastroenterol Hepatol Bed Bench. 2015 Spring;8(2):117-22.
2
The relationship between asymptomatic organ damage, and serum soluble tumor necrosis factor-like weak inducer of apoptosis (sTWEAK) and Interleukin-17A (IL-17A) levels in non-diabetic hypertensive patients.非糖尿病高血压患者无症状器官损伤与血清可溶性肿瘤坏死因子样凋亡弱诱导剂(sTWEAK)及白细胞介素-17A(IL-17A)水平之间的关系。
BMC Nephrol. 2014 Oct 1;15:159. doi: 10.1186/1471-2369-15-159.
3
Tc17 Cells in Immunity and Systemic Autoimmunity.
免疫与系统性自身免疫中的Tc17细胞
Int Rev Immunol. 2015;34(4):318-31. doi: 10.3109/08830185.2014.954698. Epub 2014 Sep 26.
4
TWEAK: A New Player in Obesity and Diabetes.肿瘤坏死因子样弱凋亡诱导因子:肥胖和糖尿病领域的新角色。
Front Immunol. 2013 Dec 30;4:488. doi: 10.3389/fimmu.2013.00488.
5
Is TWEAK a Biomarker for Autoimmune/Chronic Inflammatory Diseases?TWEAK是自身免疫性/慢性炎症性疾病的生物标志物吗?
Front Immunol. 2013 Dec 27;4:489. doi: 10.3389/fimmu.2013.00489.
6
Sampling of proximal and distal duodenal biopsies in the diagnosis and monitoring of celiac disease.十二指肠近端和远端活检样本在乳糜泻诊断和监测中的应用。
Dig Liver Dis. 2014 Apr;46(4):323-9. doi: 10.1016/j.dld.2013.12.005. Epub 2014 Jan 4.
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IL-17 producing T cells in celiac disease: angels or devils?自身免疫性肠病中产生白细胞介素 17 的 T 细胞:是天使还是恶魔?
Int Rev Immunol. 2013 Oct-Dec;32(5-6):534-43. doi: 10.3109/08830185.2013.834898. Epub 2013 Sep 16.
8
Safety, tolerability, pharmacokinetics, and pharmacodynamics of anti-TWEAK monoclonal antibody in patients with rheumatoid arthritis.类风湿关节炎患者抗 TWEAK 单克隆抗体的安全性、耐受性、药代动力学和药效学。
Clin Ther. 2013 Aug;35(8):1137-49. doi: 10.1016/j.clinthera.2013.06.008. Epub 2013 Aug 6.
9
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Clin Immunol. 2013 Apr;147(1):40-49. doi: 10.1016/j.clim.2013.02.012. Epub 2013 Feb 28.
10
Intestinal T-cell responses in celiac disease - impact of celiac disease associated bacteria.乳糜泻中的肠道 T 细胞反应——乳糜泻相关细菌的影响。
PLoS One. 2013;8(1):e53414. doi: 10.1371/journal.pone.0053414. Epub 2013 Jan 9.