Cytolytic activity against allogeneic human endothelia: resistance of cytomegalovirus-infected cells and virally activated lysis of uninfected cells.
Cytolytic activity against allogeneic human endothelia: resistance of cytomegalovirus-infected cells and virally activated lysis of uninfected cells.
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针对同种异体人内皮细胞的细胞溶解活性：巨细胞病毒感染细胞的抗性和未感染细胞的病毒激活裂解。
DOI：
10.1097/00007890-199807150-00011
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发表时间：
1998
期刊：
影响因子：
6.2
通讯作者：
Adams,PW
中科院分区：
文献类型：
--
作者：
Waldman,WJ;Knight,DA;Adams,PW
背景：巨细胞病毒（CMV）被认为是移植血管硬化发展的加重因子，然而，其具体的病因机制仍不清楚。基于我们以前的观察，CMV感染的内皮细胞（EC）刺激增殖和细胞因子的产生，同种异体T细胞，我们现在测试的假设，CMV驱动的细胞溶解活性可能有助于移植endothelial injuries.Methods的限制稀释的CMV血清阳性或血清阴性供体来源的T细胞刺激CMV感染或未感染的同种异体EC中存在的白细胞介素-2。通过[3 H]胸苷掺入试验监测T细胞增殖，并通过51 Cr释放试验检测刺激的T细胞对CMV感染或未感染的放射性标记EC靶标的裂解活性。自然杀伤（NK）细胞的活性进行了检查，通过孵育新鲜分离的外周血单个核细胞与51铬标记的目标，然后由放射性标记release.Results. CMV感染的内皮细胞是T细胞和NK细胞介导的细胞溶解的抵抗，无论捐助者血清状态，性质的刺激，或T细胞增殖的水平。相反，尽管未感染的内皮细胞不受NK细胞的伤害，这些目标经历了显着的溶解与未感染或CMV感染的ECs.Conclusions刺激T细胞。这些结果牵连CMV感染的移植物内皮细胞作为一个持久的来源感染性病毒，慢性刺激潜在的破坏性宿主炎症活动，和一个潜在的触发器产生溶解性损伤未感染的旁观者内皮细胞，提示该病毒可能扰乱移植物/宿主界面平衡的多种机制。
Background.Cytomegalovirus (CMV) has been implicated as an exacerbating agent in the development of transplant vascular sclerosis; however, specific etiologic mechanisms remain unresolved. Based upon our previous observations that CMV-infected endothelial cells (ECs) stimulate proliferation and cytokine production by allogeneic T cells, we now test the hypothesis that CMV-driven cytolytic activity may contribute to graft endothelial injury.Methods.Limiting dilutions of CMV-seropositive or-seronegative donor-derived T cells were stimulated with CMV-infected or uninfected allogeneic ECs in the presence of interleukin-2. T-cell proliferation was monitored by assay of [3 H] thymidine incorporation and stimulated T cells were tested for lytic activity against CMV-infected or uninfected radiolabeled EC targets by 51 Cr release assay. Natural killer (NK) cell activity was examined by incubating freshly isolated peripheral blood mononuclear cells with 51 Cr-labeled targets, followed by assay of radiolabel release.Results.CMV-infected ECs were resistant to T cell-and NK-mediated cytolysis regardless of donor serostatus, nature of stimulation, or level of T-cell proliferation. In contrast, although uninfected ECs were unharmed by NK cells, these targets experienced significant lysis by T cells stimulated with either uninfected or CMV-infected ECs.Conclusions.These results implicate CMV-infected graft endothelium as a persistent source of infectious virus, a chronic stimulus for potentially destructive host inflammatory activity, and a potential trigger for the generation of lytic injury to uninfected bystander endothelia, suggesting multiple mechanisms by which this virus might perturb equilibrium at the graft/host interface.
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影响因子：
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作者：
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DOI：
--
发表时间：
1994-04
期刊：
The American journal of pathology
影响因子：
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作者：
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DOI：
--
发表时间：
1995
期刊：
The American journal of pathology.
影响因子：
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作者：
Gulizia,JM;Kandolf,R;Kendall,TJ;Thieszen,SL;Wilson,JE;Radio,SJ;Costanzo,MR;Winters,GL;Miller,LL;McManus,BM
通讯作者：
McManus,BM
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影响因子：
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作者：
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通讯作者：
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