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紫外线B照射与巨细胞病毒感染协同作用,诱导52-kD/Ro抗原在细胞表面表达。

Ultraviolet B irradiation and cytomegalovirus infection synergize to induce the cell surface expression of 52-kD/Ro antigen.

作者信息

Zhu J

机构信息

Department of Medicine, McGill University, Montreal General Hospital Research Institute, Quebec, Canada.

出版信息

Clin Exp Immunol. 1996 Jan;103(1):47-53. doi: 10.1046/j.1365-2249.1996.00912.x.

Abstract

Cultured human fibroblasts (MRC-5) have been previously demonstrated to express calreticulin, but not Ro autoantigen, on their surface after human cytomegalovirus (CMV) infection. The present study addresses the question of whether other stimuli, alone or in combination with CMV, can induce the surface expression of Ro autoantigens on human fibroblasts. Using a fixed-cell ELISA to detect autoantigen expression, a synergistic effect between ultraviolet B (UVB) exposure and CMV infection on the surface expression of 52-kD/Ro antigen, but not 60-kD/Ro or calreticulin, was observed. The enhanced expression of 52-kD/Ro antigen was significant and specific, compared with untreated cells, cells infected with CMV alone or irradiated with UVB only, and cells subjected to other treatments, such as low pH. Immunofluorescence studies confirmed these findings and indicated that cells expressed 52-kD/Ro protein on their surface at 24 h after a combined UVB and CMV treatment. These studies provide evidence that synergy between UVB irradiation and CMV infection may play a role in the induction of cell surface expression of the human autoantigen, 52-kD/Ro.

摘要

先前已证明,人巨细胞病毒(CMV)感染后,培养的人成纤维细胞(MRC-5)表面会表达钙网蛋白,但不表达Ro自身抗原。本研究探讨了其他刺激因素单独或与CMV联合作用时,是否能诱导人成纤维细胞表面Ro自身抗原的表达。通过使用固定细胞酶联免疫吸附测定(ELISA)来检测自身抗原的表达,发现紫外线B(UVB)照射与CMV感染对52-kD/Ro抗原的表面表达具有协同作用,但对60-kD/Ro或钙网蛋白则无此作用。与未处理的细胞、单独感染CMV的细胞、仅接受UVB照射的细胞以及接受其他处理(如低pH)的细胞相比,52-kD/Ro抗原的表达增强具有显著性和特异性。免疫荧光研究证实了这些发现,并表明在UVB和CMV联合处理24小时后,细胞表面表达了52-kD/Ro蛋白。这些研究提供了证据,表明UVB照射与CMV感染之间的协同作用可能在诱导人自身抗原52-kD/Ro的细胞表面表达中发挥作用。

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