首页> 外文期刊>Yonsei Medical Journal >Virulent Treponema pallidum 47 kDa antigen regulates the expression of cell adhesion molecules and binding of T-lymphocytes to cultured human dermal microvascular endothelial cells
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Virulent Treponema pallidum 47 kDa antigen regulates the expression of cell adhesion molecules and binding of T-lymphocytes to cultured human dermal microvascular endothelial cells

机译:毒性梅毒螺旋体47 kDa抗原调节细胞粘附分子的表达以及T淋巴细胞与培养的人皮肤微血管内皮细胞的结合

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Perivasculitis and endothelial cell abnormalities are prominent histopathologic features of syphilis. Various cutaneous lesions are the main clinical features of syphilis. We examined whether Treponema pallidum 47 kDa antigen regulates the expression of cell adhesion molecules on human dermal microvascular endothelial cells (HDMEC) and the regulation of T-lymphocytes binding to HDMEC. Using immunofluorescence flow cytometry and enzyme-linked immunosorbent assay (ELISA), we demonstrated that T. pallidum upregulated the expression of adhesion molecules, including intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1) and E-selectin. The 47 kDa antigen of T. pallidum also activated endothelium as measured by the upregulation of the expression of adhesion molecules on HDMEC, and it also promoted an increased adherence of T-lymphocytes to HDMEC. The expressions of ICAM-1 and VCAM-1 on HDMEC and the adherence of T-lymphocytes to HDMEC were inhibited by treatment with anti-TNF-α antibody or anti-IL-1α antibody. These results show that T. pallidum or T. pallidum -specific 47 kDa antigen are capable of stimulating HDMEC to increase the expression of ICAM-1, VCAM-1 and E-selectin and thereby, promote the adherence of T-lymphocytes. The whole process may play an important role in the immunopathogenesis of syphilis and it is likely that TNF-α and IL-1α are involved.
机译:周围性皮炎和内皮细胞异常是梅毒的主要组织病理学特征。各种皮肤病变是梅毒的主要临床特征。我们检查了梅毒螺旋体47 kDa抗原是否调节人皮肤微血管内皮细胞(HDMEC)上细胞粘附分子的表达以及与HDMEC结合的T淋巴细胞的调节。使用免疫荧光流式细胞仪和酶联免疫吸附测定(ELISA),我们证明了苍白螺旋体上调了粘附分子的表达,包括细胞间粘附分子1(ICAM-1),血管细胞粘附分子1(VCAM-1)和E -选择素。苍白衣原体的47 kDa抗原还通过上调HDMEC上粘附分子的表达来激活内皮,并且还促进T淋巴细胞对HDMEC的粘附增加。用抗TNF-α抗体或抗IL-1α抗体处理可抑制HDMEC上ICAM-1和VCAM-1的表达以及T淋巴细胞对HDMEC的粘附。这些结果表明,梅毒螺旋体或梅毒螺旋体特异的47kDa抗原能够刺激HDMEC以增加ICAM-1,VCAM-1和E-选择素的表达,从而促进T淋巴细胞的粘附。整个过程可能在梅毒的免疫发病机制中起重要作用,并且可能涉及了TNF-α和IL-1α。

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