巨细胞病毒感染细胞的免疫原性分析

Immunogenecity of cytomegalovirus-infected fibroblasts

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。

AIM： To analyze the capability of cytomegalovirus （CMV）-infected human embryonic lung fibroblasts （HELFs） to induce immune response. METHODS： HELFs were infected with cytomegalovirus and stained with antibody against HLA-A2 molecular, the expression of HLA-A2 was detected by FCM. The infected HELFs were incubated with individual pp65 peptide NLVPMVATV. While the uninfected and unloaded infected HELFs served as control respectively. After PBMC was added to the differently treated HELFs and incubated, the immune response was measured with IFN-γ release as readout. RESULTS： The expression of HLA-A molecular on infected fibroblasts diminished markedly compared with that on the uninfected. The peptides expressed on the infected HELFs together with those pulsed externally induced a stronger response than the infected HELFs alone. CONCLUSION： Although CMV can downregulate the expression of MHC Ⅰ on the infected cells, it can not decrease the capacity of cells to present peptides loaded externally, and therefore still induce immune response to some extent.