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小肠结肠炎耶尔森菌O:3血清型可改变人单核细胞上血清学HLA - B27表位的表达。

Yersinia enterocolitica serotype O:3 alters the expression of serologic HLA-B27 epitopes on human monocytes.

作者信息

Wuorela M, Jalkanen S, Kirveskari J, Laitio P, Granfors K

机构信息

Department in Turku, National Public Health Institute, University of Turku, Finland.

出版信息

Infect Immun. 1997 Jun;65(6):2060-6. doi: 10.1128/iai.65.6.2060-2066.1997.

Abstract

The expression of serologic HLA-B27 epitopes on leukocytes of patients with reactive arthritis or ankylosing spondylitis has been shown to be modified in the course of the disease. The purpose of this work was to study whether phagocytosis of arthritis-triggering microbes in vitro alters the expression of HLA-B27 molecules on human antigen-presenting cells and to characterize the underlying mechanisms. Human monocytes and HLA-B27- or HLA-A2-transfected human U-937 cells were exposed to Yersinia enterocolitica serotype O:3. The expression of different epitopes of HLA-B27 was monitored by using immunofluorescence, and their synthesis was determined by quantitative immunoprecipitation. Our results show that phagocytosis of Y. enterocolitica serotype O:3 changed the expression of serological HLA-B27 epitopes. This was due to the reduced synthesis of HLA-B27 molecules. The expression of especially the epitopes which depend on the presence of peptides in the antigen-binding groove was changed. The expression of the ME1 epitope, which has been shown to be important for T-cell recognition in patients with reactive arthritis, was decreased. Down-regulation of epitopes important for the T-cell recognition may impair the elimination of arthritis-triggering microbes and lead to persistent infection. In addition, Y. enterocolitica serotype O:3 seemed to alter the repertoire of peptides presented by the HLA-B27 molecules on human monocytes. This may have a role in the pathogenesis of reactive arthritis via an autoimmune mechanism.

摘要

反应性关节炎或强直性脊柱炎患者白细胞上血清学HLA - B27表位的表达已被证明在疾病过程中会发生改变。这项研究的目的是探讨体外关节炎触发微生物的吞噬作用是否会改变人类抗原呈递细胞上HLA - B27分子的表达,并阐明其潜在机制。将人类单核细胞以及转染了HLA - B27或HLA - A2的人类U - 937细胞暴露于肠炎耶尔森菌O:3血清型。通过免疫荧光监测HLA - B27不同表位的表达,并通过定量免疫沉淀法测定其合成。我们的结果表明,肠炎耶尔森菌O:3血清型的吞噬作用改变了血清学HLA - B27表位的表达。这是由于HLA - B27分子合成减少所致。特别是那些依赖于抗原结合槽中肽段存在的表位的表达发生了变化。已证明对反应性关节炎患者T细胞识别重要的ME1表位的表达降低。对T细胞识别重要的表位下调可能会损害对关节炎触发微生物的清除,并导致持续感染。此外,肠炎耶尔森菌O:3血清型似乎改变了人类单核细胞上HLA - B27分子呈递的肽库。这可能通过自身免疫机制在反应性关节炎的发病机制中起作用。

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