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目的:检测细胞感染巨细胞病毒后诱导免疫应答的能力。方法:将巨细胞病毒感染人胚肺成纤维母细胞(HELF),抗体标记细胞表面HLA-A2分子,流式细胞术(FCM)检测感染细胞HLA-A02表达强度;将感染的HELF、荷载外源性多肽的自身PBMC以及未感染的HELF,分别与PBMC共同孵育,FCM检测CD8+T细胞内IFN-γ的表达作为应答指标。结果:感染细胞HLA-A分子表达强度较未感染组降低78.24%±19.72%。感染并荷载外源性多肽的HELF诱导产生的刺激应答率,高于单纯巨细胞病毒感染的HELF和荷载多肽的未感染HELF所诱导应答比率。结论:尽管巨细胞病毒下调MHCI分子表达,但可能不减弱细胞递呈外源多肽的能力,并足以诱导产生免疫应答。
Objective: To test the ability of cells to induce immune response after infection with cytomegalovirus. Methods: The expression of HLA-A02 in infected cells was detected by infection of cytomegalovirus (HELF), HLA-A2 molecules on the surface of antibody labeled cells and flow cytometry (FCM). The infected HELF, The self-PBMC of PBMC and uninfected HELF were co-incubated with PBMC, and the expression of IFN-γ in CD8 + T cells was detected by FCM as a response indicator. Results: The expression of HLA-A in infected cells was 78.24% ± 19.72% lower than that in non-infected cells. The response rate of HELF induced by infected and loaded exogenous peptides was higher than that induced by cytomegalovirus infected HELF and unloaded HELF. CONCLUSIONS: Although cytomegalovirus down-regulates MHC I expression, it may not attenuate the cells’ ability to deliver exogenous peptides and is sufficient to induce an immune response.