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麻疹病毒感染中的免疫损伤。III. 人细胞毒性淋巴细胞的存在及特性

Immunologic injury in measles virus infection. III. Presence and characterization of human cytotoxic lymphocytes.

作者信息

Perrin L H, Tishon A, Oldstone M B

出版信息

J Immunol. 1977 Jan;118(1):282-90.

PMID:830751
Abstract

Human peripheral blood leukocytes (PBL) from patients with chronic measles virus infection (SSPE) or from immune, adult humans (convalescent from acute childhood measles virus infection) are cytotoxic for target cells infected with measles virus as measured by a 51Cr assay. Specific release of 51Cr by immune PBL occurred both with and without human antibodies added to measles virus-infected cultures. Maximal killing in the absence of added antibodies to measles virus was usually detected only after 15 to 18 hr of incubation and with a high PBL to target ratio (100:1). When antibody to measles virus was added, PBL-mediated killing of virus-infected cells was not blocked. Instead, killing was enhanced and maximal lysis occurred with fewer PBL and a shorter incubation time. This cytotoxic reaction was inhibited in a dose-response manner upon the addition of Fab fragments of IgG containing antibodies to measles virus. On the average 4 to 5 x 105 antibody molecules bound per infected target cell before initiation of antibody-enhanced PBL killing. Depletion of either glass-adhering or E-rosette-forming cells did not reduce PBL killing of measles virus-infected target cells in either system. In contrast, removal of non-E rosette or of EAC rosette-forming population of PBL almost completely abrogated cytotoxicity. When Fc-bearing cells were removed, killing of virus-infected target cells was concomitantly reduced. Lysis of measles virus-infected target cells did not require histocompatibility between the PBL and the target cell. Further, immunospecific lymphocyte killing was not enhanced by such a histocompatibility fit. These experiments indicate first, that the effector PBL involved in lysis of measles virus-infected targets are not T cells but are probably K cells and, second, that PBL obtained from patients with SSPE are competent in killing measles virus-infected targets. Moreover, sera from SSPE patients did not contain a factor(s) that blocked PBL-mediated cytotoxicity.

摘要

通过51Cr释放试验检测发现,慢性麻疹病毒感染患者(亚急性硬化性全脑炎,SSPE)或免疫的成年人(急性儿童期麻疹病毒感染康复者)的人外周血白细胞(PBL)对感染麻疹病毒的靶细胞具有细胞毒性。无论是否向感染麻疹病毒的培养物中添加人抗体,免疫PBL均可特异性释放51Cr。在不添加抗麻疹病毒抗体的情况下,通常仅在孵育15至18小时后,且PBL与靶细胞比例较高(100:1)时,才能检测到最大杀伤作用。添加抗麻疹病毒抗体后,PBL介导的病毒感染细胞杀伤作用并未被阻断。相反,杀伤作用增强,且用较少的PBL和较短的孵育时间即可出现最大程度的裂解。加入含有抗麻疹病毒抗体的IgG Fab片段后,这种细胞毒性反应呈剂量反应性抑制。在抗体增强的PBL杀伤作用开始前,每个感染的靶细胞平均结合4至5×105个抗体分子。在这两种系统中,去除玻璃黏附细胞或E花环形成细胞均不会降低PBL对感染麻疹病毒靶细胞的杀伤作用。相比之下,去除PBL的非E花环或EAC花环形成群体几乎可完全消除细胞毒性。去除携带Fc的细胞后,病毒感染靶细胞的杀伤作用随之降低。麻疹病毒感染靶细胞的裂解并不要求PBL与靶细胞之间具有组织相容性。此外,这种组织相容性匹配并不会增强免疫特异性淋巴细胞的杀伤作用。这些实验首先表明,参与裂解感染麻疹病毒靶细胞的效应PBL不是T细胞,而可能是K细胞;其次表明,从SSPE患者获得的PBL能够杀伤感染麻疹病毒的靶细胞。此外,SSPE患者的血清中不存在阻断PBL介导的细胞毒性的因子。

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