Immune control of SV40-induced tumors in mice.
Immune control of SV40-induced tumors in mice.
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SV40 诱导的小鼠肿瘤的免疫控制。
DOI：
10.1002/ijc.2910390612
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发表时间：
1987
影响因子：
6.4
通讯作者：
Knowles,BB
中科院分区：
文献类型：
--
作者：
Pan,S;Abramczuk,J;Knowles,BB
小鼠对SV 40 T抗原产生细胞毒性T淋巴细胞（CTL）免疫应答的能力由宿主的H-2单倍型决定; H-2 bandk小鼠为高应答者，H-2 d小鼠为低应答者。用SV 40攻击这3种H-2单倍型的小鼠，发现它们产生和维持对SV 40 T-抗原的抗体应答的能力相当。为了研究宿主免疫应答的不同组分在控制SV 40诱导的肿瘤生长中的作用，评估了新鲜建立的细胞系的致瘤潜力，所述细胞系通过对来自6种H-2单倍型的近交系小鼠的正常组织的细胞进行SV 40转化而获得。每种细胞系在无胸腺和新生小鼠中具有致瘤性，但在成年同基因免疫活性小鼠中不具有致瘤性。然后将来自这些初始SV 40转化系的细胞在无胸腺（nu/nu）小鼠中传代，在体外重建，并再次转移到同基因动物中。将H-2dSV 40转化体转移到H-2d单倍型的低应答或无应答小鼠中导致一些动物中的肿瘤形成。来自这些肿瘤的细胞表达病毒编码的T抗原和H-2D限制元件。此外，患有肿瘤的动物的比例随其对与H-2Dd相关的SV 40 T抗原的CTL应答强度而变化。因此，在H-2d动物中，肿瘤细胞的生长似乎是由于细胞从无效的CTL监视中逃逸所致。通过将体内选择的H-2bor H-2kSV 40转化体转移到同基因高应答小鼠中，没有形成肿瘤。因此，我们研究了CTL在选择能够逃避免疫监视的SV 40转化细胞中的作用。在通过CTL进行严格免疫选择的条件下，获得不再表达相关H-2 I类限制性元件的致瘤细胞。尽管各种免疫效应机制之间的相互作用可能在SV 40转化体的识别和消除中发挥作用，但我们的结果与SV 40特异性CTL应答是SV 40肿瘤生长的主要控制的假设一致。
The ability of mice to mount a cytotoxic T‐lymphocyte (CTL) immune response to SV40 T‐antigen is determined by the H‐2 haplotype of the host; H‐2bandkmice are high responders and H‐2dmice are low responders. Mice of these 3 H‐2 haplotypes were challenged with SV40 and their ability to generate and sustain an antibody response to SV40 T‐antigen was found to be equivalent. To investigate the role of the different components of the host immune response in controlling growth of SV40‐induced tumors, the tumorigenic potential of freshly established cell lines, obtained by SV40 transformation of cells from normal tissues of inbred strains of mice of 6 H‐2 haplotypes, was assessed. Each cell line was tumorigenic in athymic and newborn mice but not in adult syngeneic immunocompetent mice. Cells from these initial SV40‐transformed lines were then passaged in athymic (nu/nu) mice, re‐establishedin vitroand again transferred into syngeneic animals. Transfer of H‐2dSV40 transformants to low or non‐responder mice of the H‐2dhaplotype resulted in tumor formation in some animals. Cells derived from these tumors expressed both the viral encoded T‐antigen and the H‐2Ddrestriction element. Furthermore, the proportion of animals with tumors varied with the strength of their CTL‐responsiveness to SV40 T‐antigen in association with H‐2Dd. Therefore, in H‐2danimals, tumor cell growth appears to result from escape of cells from inefficient CTL surveillance. No tumors were formed by transfer of thein vivoselected H‐2bor H‐2kSV40 transformants to syngeneic high‐responder mice. We therefore investigated the role of CTL in the selection of SV40‐transformed cells able to escape immune surveillance. Under conditions of stringent immune selection by CTLs, tumorigenic cells that no longer expressed the relevant H‐2 class‐I restriction element were obtained. Although interaction between the various immune effector mechanisms may play a role in the recognition and elimination of SV40 transformants, our results were consistent with the hypothesis that the SV40‐specific CTL response is the predominant control of SV40 tumor growth.
移植耐受中的再循环、抑制性 T 细胞
影响因子：
15.3
作者：
Susan Dorsch;Bruce Roser
通讯作者：
Bruce Roser
用 SV40 病毒体外转化的 C3H 成纤维细胞的进行性肿瘤的表征。
DOI：
--
发表时间：
1982
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Gooding,LR
通讯作者：
Gooding,LR
影响因子：
64.8
作者：
BILLINGHAM, RE;BRENT, L;MEDAWAR, PB
通讯作者：
MEDAWAR, PB