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病毒诱导的大鼠骨肉瘤的生物学、病理学及免疫学。II. 免疫学研究。

The biology, pathology and immunology of a virus induced rat osteosarcoma. II. Immunological studies.

作者信息

Czitrom A A, Langer F, Gross A E, Urovitz E P, Pritzker K P

出版信息

Int Orthop. 1980;4(3):167-75. doi: 10.1007/BF00268153.

Abstract

The immunogenicity of a virus-induced rat osteosarcoma was studied utilizing the lymphocyte microcytoxicity test. Lymphocytes from "progressor" animals (in which the tumour progressed and metastasized) demonstrated an ability to kill osteosarcoma cells in vitro, while serum from these animals abrogated or blocked the cell-mediated cytotoxicity. Lymphocytes from "regressor" animals (in which tumours failed to develop or regressed spontaneously) also showed cytolytic activity against osteosarcoma cells in vitro, but their serum failed to block the lymphocyte-mediated cytolysis. Both progressor and regressor animals demonstrated the presence of humoral cytotoxic antibodies to tumour antigens on the basis of the ability of their serum to kill tumour cells in vitro. In an attempt to alter the fatal course of the disease in progressor animals, immunoprophylaxis and immunotherapy of the osteosarcoma in F1 hybrid rats war carried out by injecting them with parentalor, third party, allogeneic lymphoid cells. Injection of parental spleen lymphocytes into F1 hybrids produced a transient graft versus host reaction (GVHR), and prolonged the survival of the animals when lymphocytes were injected three days before, seven days after and on the day of tumour induction. Injection of allogeneic, third party lymphoid cells produced no detectable GVHR and prolonged the survival of F1 hybrids with osteosarcoma only when injected on the day of tumour induction. The prolonged survival of the groups treated with parental lymphoid cells was a result of stimulation of the host's immunological mechanisms during a transient GVHR, whereas the prolongation of survival in the group given allogeneic cells was most likely the result of a direct action of the donor lymphocytes on tumour cells, and not connected to a GVHR.

摘要

利用淋巴细胞微细胞毒性试验研究了病毒诱导的大鼠骨肉瘤的免疫原性。来自“进展型”动物(肿瘤进展并发生转移)的淋巴细胞在体外表现出杀伤骨肉瘤细胞的能力,而这些动物的血清则消除或阻断了细胞介导的细胞毒性。来自“消退型”动物(肿瘤未能生长或自发消退)的淋巴细胞在体外也表现出对骨肉瘤细胞的溶细胞活性,但其血清未能阻断淋巴细胞介导的细胞溶解。基于其血清在体外杀伤肿瘤细胞的能力,进展型和消退型动物均显示存在针对肿瘤抗原的体液细胞毒性抗体。为了改变进展型动物疾病的致命进程,通过给F1杂种大鼠注射亲代或第三方同种异体淋巴细胞,对骨肉瘤进行了免疫预防和免疫治疗。向F1杂种大鼠注射亲代脾淋巴细胞会产生短暂的移植物抗宿主反应(GVHR),并且在肿瘤诱导前三天、后七天和当天注射淋巴细胞时可延长动物的存活时间。注射同种异体第三方淋巴细胞未产生可检测到的GVHR,并且仅在肿瘤诱导当天注射时才延长了患有骨肉瘤的F1杂种大鼠的存活时间。用亲代淋巴细胞治疗的组存活时间延长是短暂GVHR期间宿主免疫机制受到刺激的结果,而给予同种异体细胞的组存活时间延长最可能是供体淋巴细胞直接作用于肿瘤细胞的结果,与GVHR无关。

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