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Br J Cancer. 1989 Sep;60(3):351-7. doi: 10.1038/bjc.1989.284.
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Potentiation of delayed-type hypersensitivity response to syngeneic tumors in mice prevaccinated with cells modified by hydrostatic pressure and crosslinking.用流体静压和交联修饰的细胞预接种的小鼠对同基因肿瘤的迟发型超敏反应增强。
Cancer Immunol Immunother. 1991;33(1):1-8. doi: 10.1007/BF01742520.

本文引用的文献

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Somatic Cell Genet. 1982 Sep;8(5):635-42. doi: 10.1007/BF01542856.
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Induction of delayed-type hypersensitivity and antitumor immunity by systemic BCG.全身性卡介苗诱导迟发型超敏反应和抗肿瘤免疫
Cell Immunol. 1980 Mar 1;50(1):136-52. doi: 10.1016/0008-8749(80)90013-1.
3
Fluorescence analysis and anatomic distribution of mouse T lymphocyte subsets defined by monoclonal antibodies to the antigens Thy-1, Lyt-1, Lyt-2, and T-200.用针对Thy-1、Lyt-1、Lyt-2和T-200抗原的单克隆抗体对小鼠T淋巴细胞亚群进行的荧光分析及解剖学分布
J Immunol. 1981 Dec;127(6):2594-604.
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Mechanisms of anti-tumor action of Corynebacterium parvum. I. Potentiated tumor-specific immunity and its therapeutic limitations.短小棒状杆菌的抗肿瘤作用机制。I. 增强的肿瘤特异性免疫及其治疗局限性。
J Exp Med. 1981 Sep 1;154(3):609-20. doi: 10.1084/jem.154.3.609.
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H-2-restricted recognition of minor histocompatibility antigens in delayed type hypersensitivity.迟发型超敏反应中H-2限制性对次要组织相容性抗原的识别
J Immunogenet. 1980 Aug;7(4):315-24. doi: 10.1111/j.1744-313x.1980.tb00725.x.
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Delayed cutaneous hypersensitivity to autologous tumor cells in colorectal cancer patients immunized with an autologous tumor cell: Bacillus Calmette-Guérin vaccine.用自体肿瘤细胞-卡介苗疫苗免疫的结直肠癌患者对自体肿瘤细胞的迟发型皮肤超敏反应。
Cancer Res. 1984 Apr;44(4):1671-6.
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A Rauscher-virus-induced T-lymphocyte cell line. Induction of differentiation under influence of dimethylsulfoxide and phorbolesters.一种劳舍尔病毒诱导的T淋巴细胞系。在二甲基亚砜和佛波酯影响下的分化诱导。
Int J Cancer. 1983 Oct 15;32(4):501-6. doi: 10.1002/ijc.2910320418.
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Immunologic mechanisms in UV radiation carcinogenesis.紫外线辐射致癌中的免疫机制。
Adv Cancer Res. 1981;34:69-106. doi: 10.1016/s0065-230x(08)60239-0.
9
Induction of Ia and H-2 antigens on a macrophage cell line by immune interferon.免疫干扰素对巨噬细胞系Ia和H-2抗原的诱导作用。
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10
In vitro production of immunosuppressive factors by murine sarcoma virus-transformed mouse fibroblasts.鼠肉瘤病毒转化的小鼠成纤维细胞体外产生免疫抑制因子。
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对劳氏鼠白血病病毒诱导的肿瘤细胞系迟发型超敏反应的增强与抑制

Enhancement and suppression of DTH reactivity to Rauscher murine leukaemia virus induced tumour cell lines.

作者信息

Knulst A C, Berends D, Bazuin C, van Rooij H C, de Both N J, Benner R

机构信息

Department of Cell Biology, Erasmus University, Rotterdam, The Netherlands.

出版信息

Br J Cancer. 1989 Sep;60(3):351-7. doi: 10.1038/bjc.1989.284.

DOI:10.1038/bjc.1989.284
PMID:2477052
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2247201/
Abstract

Delayed-type hypersensitivity (DTH) to Rauscher murine leukaemia virus (R-MuLV) encoded or induced determinants was induced in mice by three syngeneic R-MuLV-induced tumour cell lines, i.e. a myeloid tumour, RMB-1, an erythroid tumour, RED-1, and a lymphoid tumour, RLD-1. DTH to subcutaneously (s.c.) administered RMB-1 cells appeared on day 4, with a maximum DTH response on day 6 or 7. The induction of DTH could be prevented by intravenous (i.v.) pre-immunisation with R-MuLV-induced tumour cells several days before the s.c. immunisation. The three R-MuLV-induced tumour cell lines showed cross-reactivity in the DTH assay, whereas no cross-reactivity was found with syngeneic WEHI-3 cells. This indicates that the three R-MuLV-induced tumour cell lines share a virally encoded or induced antigenic determinant, which activates T-cells. When the RMB-1 cells used for immunisation had been cultured in medium supplemented with interferon-gamma (IFN-gamma), the subsequent DTH response was increased. This coincided with an increased expression of the R-MuLV-specific antigenic determinants on RMB-1 cells as demonstrated by Scatchard analysis. Furthermore, IFN-gamma increased the MHC class I antigen expression on RMB-1 cells, whereas the class II antigen expression remained undetectable.

摘要

通过三种同基因的劳舍尔鼠白血病病毒(R-MuLV)诱导的肿瘤细胞系,即一种髓系肿瘤细胞系RMB-1、一种红系肿瘤细胞系RED-1和一种淋巴系肿瘤细胞系RLD-1,在小鼠中诱导出对R-MuLV编码或诱导的决定簇的迟发型超敏反应(DTH)。对皮下注射的RMB-1细胞的DTH反应在第4天出现,在第6天或第7天达到最大DTH反应。在皮下免疫前几天通过静脉注射用R-MuLV诱导的肿瘤细胞进行预免疫,可以预防DTH的诱导。这三种R-MuLV诱导的肿瘤细胞系在DTH试验中表现出交叉反应性,而与同基因的WEHI-3细胞没有交叉反应性。这表明这三种R-MuLV诱导的肿瘤细胞系共享一种病毒编码或诱导的抗原决定簇,该决定簇可激活T细胞。当用于免疫的RMB-1细胞在补充有γ干扰素(IFN-γ)的培养基中培养时,随后的DTH反应增强。如Scatchard分析所示,这与RMB-1细胞上R-MuLV特异性抗原决定簇表达的增加相一致。此外,IFN-γ增加了RMB-1细胞上MHC I类抗原的表达,而II类抗原表达仍未检测到。