细胞与分子免疫学杂志
細胞與分子免疫學雜誌
세포여분자면역학잡지
2009年
10期
907-909,913
,共4页
王延军%孙斌%刘道洁%武彦宁%赵敬敬
王延軍%孫斌%劉道潔%武彥寧%趙敬敬
왕연군%손빈%류도길%무언저%조경경
巨细胞病毒%特异性免疫应答%免疫原性%抗原递呈%移植
巨細胞病毒%特異性免疫應答%免疫原性%抗原遞呈%移植
거세포병독%특이성면역응답%면역원성%항원체정%이식
cytomegalovirus%specific immune response%immunogenecity%antigen presentation%transplantation
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MHC Ⅰ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.
目的:檢測細胞感染巨細胞病毒後誘導免疫應答的能力.方法:將巨細胞病毒感染人胚肺成纖維母細胞(HELF),抗體標記細胞錶麵HLA-A2分子,流式細胞術(FCM)檢測感染細胞HLA-A02錶達彊度;將感染的HELF、荷載外源性多肽的自身PBMC以及未感染的HELF,分彆與PBMC共同孵育,FCM檢測CD8~+T細胞內IFN-γ的錶達作為應答指標.結果:感染細胞HLA-A分子錶達彊度較未感染組降低78.24%±19.72%.感染併荷載外源性多肽的HELF誘導產生的刺激應答率,高于單純巨細胞病毒感染的HELF和荷載多肽的未感染HELF所誘導應答比率.結論:儘管巨細胞病毒下調MHC Ⅰ分子錶達,但可能不減弱細胞遞呈外源多肽的能力,併足以誘導產生免疫應答.
목적:검측세포감염거세포병독후유도면역응답적능력.방법:장거세포병독감염인배폐성섬유모세포(HELF),항체표기세포표면HLA-A2분자,류식세포술(FCM)검측감염세포HLA-A02표체강도;장감염적HELF、하재외원성다태적자신PBMC이급미감염적HELF,분별여PBMC공동부육,FCM검측CD8~+T세포내IFN-γ적표체작위응답지표.결과:감염세포HLA-A분자표체강도교미감염조강저78.24%±19.72%.감염병하재외원성다태적HELF유도산생적자격응답솔,고우단순거세포병독감염적HELF화하재다태적미감염HELF소유도응답비솔.결론:진관거세포병독하조MHC Ⅰ분자표체,단가능불감약세포체정외원다태적능력,병족이유도산생면역응답.
AIM: To analyze the capability of cytomegaIovirus (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.