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本文引用的文献

1
Over-expression of the decoy receptor 3 (DcR3) gene in peripheral blood mononuclear cells (PBMC) derived from silicosis patients.矽肺病患者外周血单个核细胞（PBMC）中诱饵受体3（DcR3）基因的过表达。
Clin Exp Immunol. 2000 Feb;119(2):323-7. doi: 10.1046/j.1365-2249.2000.01132.x.
2
Serum levels of soluble Fas ligand in patients with silicosis.矽肺患者血清中可溶性Fas配体水平
Clin Exp Immunol. 1999 Dec;118(3):441-4. doi: 10.1046/j.1365-2249.1999.01083.x.
3
Evaluation of cases with silicosis using the parameters related to Fas-mediated apoptosis.利用与Fas介导的细胞凋亡相关的参数对矽肺病例进行评估。
Int J Mol Med. 1999 Oct;4(4):407-11. doi: 10.3892/ijmm.4.4.407.
4
Is anti-topoisomerase I a serum marker of pulmonary involvement in systemic sclerosis?抗拓扑异构酶I是否为系统性硬化症肺部受累的血清标志物？
Chest. 1999 Sep;116(3):715-20. doi: 10.1378/chest.116.3.715.
5
Connective tissue disease and silicosis.结缔组织病与矽肺
Am J Ind Med. 1999 Apr;35(4):375-81. doi: 10.1002/(sici)1097-0274(199904)35:4<375::aid-ajim8>3.0.co;2-i.
6
Silica induced scleroderma--clinical and experimental aspects.二氧化硅诱发的硬皮病——临床与实验方面
J Rheumatol. 1998 Oct;25(10):1917-26.
7
Soluble Fas mRNA is dominantly expressed in cases with silicosis.可溶性Fas信使核糖核酸在矽肺病例中呈优势表达。
Immunology. 1998 Jun;94(2):258-62. doi: 10.1046/j.1365-2567.1998.00509.x.
8
Activation-induced cell death in human peripheral blood lymphocytes after stimulation with silicate in vitro.体外硅酸盐刺激后人外周血淋巴细胞中的活化诱导细胞死亡
Int J Oncol. 1998 Jun;12(6):1355-9. doi: 10.3892/ijo.12.6.1355.
9
Elevated soluble Fas/APO-1 (CD95) levels in silicosis patients without clinical symptoms of autoimmune diseases or malignant tumours.在没有自身免疫性疾病或恶性肿瘤临床症状的矽肺患者中，可溶性Fas/APO-1（CD95）水平升高。
Clin Exp Immunol. 1997 Nov;110(2):303-9. doi: 10.1111/j.1365-2249.1997.tb08332.x.
10
Lymphocytes, cytokines, inflammation, and immune trafficking.淋巴细胞、细胞因子、炎症与免疫细胞迁移
Curr Opin Rheumatol. 1997 Sep;9(5):380-6. doi: 10.1097/00002281-199709000-00002.

检测矽肺患者的抗拓扑异构酶 I 自身抗体。

Detection of anti-topoisomerase I autoantibody in patients with silicosis.

机构信息

Department of Hygiene, Kawasaki Medical School, 577 Matsushima, 701-0192, Kurashiki, Okayama, Japan,

出版信息

Environ Health Prev Med. 2002 Apr;7(1):7-10. doi: 10.1007/BF02898059.

DOI:10.1007/BF02898059
PMID:21432283
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2723232/
Abstract

OBJECTIVES

The aim of this study was to detect anti-topoisomerase I (anti-topo I) autoantibodies, which are known to be limited in systemic sclerosis patients, in silicosis patients with no clinical symptoms of autoimmune disease.

METHODS

Serum anti-topo I autoantibodies were detected using ELISA. Differences in clinical parameters between patients with and without anti-topo I autoantibodies were analyzed.

RESULTS

Seven of 69 patients had anti-topo I autoantibodies. These 7 patients showed elevated PaCO(2) values (P=0.0212), and inverse correlations between serum soluble Fas levels and PaCO(2) values were found.

CONCLUSION

Anti-topo I autoantibodies were detected in 10.1% of silicosis patients without any clinical symptoms of autoimmune disease. The findings here suggest that the genesis of anti-topo I autoantibodies might be related to pulmonary involvement or lung fibrosis associated with progression of silicosis.

摘要

目的

本研究旨在检测系统性硬化症患者中有限的抗拓扑异构酶 I（抗拓扑 I）自身抗体，在无自身免疫性疾病临床症状的矽肺患者中。

方法

采用 ELISA 法检测血清抗拓扑 I 自身抗体。分析有和无抗拓扑 I 自身抗体的患者之间临床参数的差异。

结果

69 例患者中有 7 例存在抗拓扑 I 自身抗体。这 7 例患者的 PaCO2 值升高（P=0.0212），并且发现血清可溶性 Fas 水平与 PaCO2 值之间存在负相关。

结论

在无任何自身免疫性疾病临床症状的矽肺患者中检测到抗拓扑 I 自身抗体。这些发现表明，抗拓扑 I 自身抗体的产生可能与矽肺进展相关的肺部受累或肺纤维化有关。