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肿瘤细胞上组织相容性抗原表达的变化:BALB.K品系中一种粗病毒诱导的白血病缺乏H-2Kk基因产物

Variation of expression of histocompatibility antigens on tumor cells: absence of H-2Kk-gene products from a gross-virus-induced leukemia in BALB.K.

作者信息

Schmidt W, Leben L, Atfield G, Festenstein H

出版信息

Immunogenetics. 1981;14(3-4):323-39. doi: 10.1007/BF00342201.

DOI:10.1007/BF00342201
PMID:7333657
Abstract

The antigenic profile of the K-GV tumor of BALB.K origin, induced by Gross virus and maintained in vitro and in vivo, was investigated by serological and immunochemical methods and techniques of cell-mediated immunity. The H-2Kk-gene products were absent by several criteria: (1) monoclonal antibody and conventional alloantisera directed against eh H-2Kk antigenic specificities were nonreactive by direct testing and by absorptions. (2) H-2Kk products could not be precipitated from glycoprotein or protein extracts of the radiolabeled K-GV tumor. (3) Cytotoxic effectors against H-2Kk produced by sensitization in vitro and in vivo failed to kill K-GV target cells. (4) The tumor could neither stimulate BALB.B congenic mice to produce cytotoxic effectors nor specific cytotoxic antibody against H-2Kk-gene products. In contrast, the H-2Dk antigen was readily detectable by all these criteria. These findings therefore describe a tumor which has selectively lost the H-2K-gene products. The K-GV tumor was able to generate Gross-virus specific CTL, but had greatly reduced susceptibility to lysis by Gross-virus specific CTL generated by H-2K expressing AKR (H-2k) tumors. These findings have important implications for the associative recognition of tumor antigens and the immune surveillance of virally induced tumors.

摘要

用血清学、免疫化学方法及细胞介导免疫技术,对由格罗斯病毒诱导并在体内外维持的BALB.K来源的K-GV肿瘤的抗原特性进行了研究。根据多项标准,H-2Kk基因产物缺失:(1)针对H-2Kk抗原特异性的单克隆抗体和传统同种异体抗血清,通过直接检测和吸收试验均无反应。(2)无法从放射性标记的K-GV肿瘤的糖蛋白或蛋白质提取物中沉淀出H-2Kk产物。(3)在体外和体内致敏产生的针对H-2Kk的细胞毒性效应细胞未能杀死K-GV靶细胞。(4)该肿瘤既不能刺激BALB.B同源基因小鼠产生细胞毒性效应细胞,也不能产生针对H-2Kk基因产物的特异性细胞毒性抗体。相比之下,通过所有这些标准都能很容易地检测到H-2Dk抗原。因此,这些发现描述了一种选择性丢失H-2K基因产物的肿瘤。K-GV肿瘤能够产生格罗斯病毒特异性CTL,但对由表达H-2K的AKR(H-2k)肿瘤产生的格罗斯病毒特异性CTL的裂解敏感性大大降低。这些发现对肿瘤抗原的联合识别以及病毒诱导肿瘤的免疫监视具有重要意义。

相似文献

1
Variation of expression of histocompatibility antigens on tumor cells: absence of H-2Kk-gene products from a gross-virus-induced leukemia in BALB.K.肿瘤细胞上组织相容性抗原表达的变化:BALB.K品系中一种粗病毒诱导的白血病缺乏H-2Kk基因产物
Immunogenetics. 1981;14(3-4):323-39. doi: 10.1007/BF00342201.
2
Resistance to cell-mediated cytotoxicity is correlated with reduction of H-2K gene products in AKR leukemia.对细胞介导的细胞毒性的抗性与AKR白血病中H-2K基因产物的减少相关。
Immunogenetics. 1982;16(3):257-64. doi: 10.1007/BF00343314.
3
Resistance to cellular immune response in AKR leukemias.AKR白血病中对细胞免疫反应的抗性。
Eur J Immunol. 1986 Jul;16(7):753-9. doi: 10.1002/eji.1830160707.
4
Viral specificity of H-2-restricted T killer cells directed against syngeneic tumors induced by Gross, Friend, or Rauscher leukemia virus.针对由格罗斯、弗里德或劳舍尔白血病病毒诱导的同基因肿瘤的H-2限制性T杀伤细胞的病毒特异性。
J Exp Med. 1979 Nov 1;150(5):1174-86. doi: 10.1084/jem.150.5.1174.
5
Cell surface expression of cytotoxic T lymphocyte-defined, AKR/Gross leukemia virus-associated tumor antigens by normal AKR.H-2b splenic B cells.正常AKR.H-2b脾B细胞对细胞毒性T淋巴细胞定义的、AKR/格罗斯白血病病毒相关肿瘤抗原的细胞表面表达。
J Immunol. 1983 Dec;131(6):3078-84.
6
The specificity of H-2-restricted cytotoxic T lymphocytes directed to AKR/Gross leukemia virus-induced tumors. I. Isolation of a selectively resistant variant tumor subclone.针对AKR/格罗斯白血病病毒诱导肿瘤的H-2限制性细胞毒性T淋巴细胞的特异性。I. 一种选择性抗性变异肿瘤亚克隆的分离。
Eur J Immunol. 1983 Nov;13(11):863-70. doi: 10.1002/eji.1830131102.
7
The specificity of H-2-restricted cytotoxic T lymphocytes directed to AKR/Gross leukemia virus-induced tumors. III. Coordinate alterations in viral gp70 antigen expression and restoration of CTL-susceptibility to insusceptible variant tumors.针对AKR/格罗斯白血病病毒诱导肿瘤的H-2限制性细胞毒性T淋巴细胞的特异性。III. 病毒gp70抗原表达的协同改变以及细胞毒性T淋巴细胞对不敏感变异肿瘤敏感性的恢复
J Immunol. 1986 Mar 15;136(6):2271-9.
8
H-2-specific antibodies induced by injection of syngeneic leukemia cells.通过注射同基因白血病细胞诱导产生的H-2特异性抗体。
Immunogenetics. 1987;25(4):215-21. doi: 10.1007/BF00404690.
9
Genetic control of the induction of cytolytic T lymphocyte responses to AKR/Gross viral leukemias. I. H-2-encoded dominant gene control.对AKR/Gross病毒性白血病细胞溶解性T淋巴细胞反应诱导的遗传控制。I. H-2编码的显性基因控制。
J Immunol. 1984 May;132(5):2658-64.
10
The specificity of H-2-restricted cytotoxic T lymphocytes directed to AKR/Gross leukemia virus-induced tumors. II. Altered gp70 display and production of noninfectious virus particles by an insusceptible variant tumor.针对AKR/格罗斯白血病病毒诱导肿瘤的H-2限制性细胞毒性T淋巴细胞的特异性。II. 一种不易感的变异肿瘤中gp70展示的改变及非感染性病毒颗粒的产生
Eur J Immunol. 1983 Nov;13(11):871-7. doi: 10.1002/eji.1830131103.

引用本文的文献

1
Resistance to cell-mediated cytotoxicity is correlated with reduction of H-2K gene products in AKR leukemia.对细胞介导的细胞毒性的抗性与AKR白血病中H-2K基因产物的减少相关。
Immunogenetics. 1982;16(3):257-64. doi: 10.1007/BF00343314.
2
Variation in p30-related proteins in gross virus-induced tumor cell lines derived from H-2 congenic mice.源自H-2同源基因小鼠的大体病毒诱导肿瘤细胞系中p30相关蛋白的变异
J Virol. 1984 Jan;49(1):14-9. doi: 10.1128/JVI.49.1.14-19.1984.
3
Evidence for H-2-linked control of retrovirus production in Friend virus-induced tumor cell lines.

本文引用的文献

1
Murine cytotoxic T-cell response to alphavirus is associated mainly withH- 2D ( k ).鼠细胞毒性 T 细胞对甲病毒的反应主要与 H-2D(k) 相关。
Immunogenetics. 1978 Dec;7(1):551-61. doi: 10.1007/BF01844044.
2
GENETIC BASIS OF SUSCEPTIBILITY TO VIRAL LEUKAEMOGENESIS.病毒致白血病易感性的遗传基础。
Lancet. 1964 Dec 5;2(7371):1207-9. doi: 10.1016/s0140-6736(64)91043-8.
3
T cell-mediated immunity to oncornavirus-induced tumors. II. Ability of different T cell sets to prevent tumor growth in vivo.T细胞介导的对致癌RNA病毒诱导肿瘤的免疫反应。II. 不同T细胞群体在体内预防肿瘤生长的能力。
H-2连锁控制Friend病毒诱导的肿瘤细胞系中逆转录病毒产生的证据。
J Virol. 1986 Jun;58(3):782-9. doi: 10.1128/JVI.58.3.782-789.1986.
4
H-2-specific antibodies induced by injection of syngeneic leukemia cells.通过注射同基因白血病细胞诱导产生的H-2特异性抗体。
Immunogenetics. 1987;25(4):215-21. doi: 10.1007/BF00404690.
5
A transcription factor interacting with the class I gene enhancer is inactive in tumorigenic cell lines which suppress major histocompatibility complex class I genes.一种与I类基因增强子相互作用的转录因子在抑制主要组织相容性复合体I类基因的致瘤细胞系中无活性。
Mol Cell Biol. 1990 Aug;10(8):4100-9. doi: 10.1128/mcb.10.8.4100-4109.1990.
J Immunol. 1980 Feb;124(2):851-4.
4
Changes in H-2 antigen expression on a murine spontaneous leukaemia (K36) detected by cell-mediated cytotoxicity assay.
J Immunogenet. 1980 Feb;7(1):19-29. doi: 10.1111/j.1744-313x.1980.tb00704.x.
5
Separate cytotoxic T lymphocyte subsets recognize the different H-2 specificities.不同的细胞毒性T淋巴细胞亚群识别不同的H-2特异性。
J Exp Med. 1980 Mar 1;151(3):773-80. doi: 10.1084/jem.151.3.773.
6
The inheritance of susceptibility to the Gross leukemia virus in mice.小鼠对格罗斯白血病病毒易感性的遗传
Genetics. 1966 Mar;53(3):529-39. doi: 10.1093/genetics/53.3.529.
7
Genetic origin of tumor antigens.肿瘤抗原的遗传起源。
Cancer Res. 1968 Jul;28(7):1280-7.
8
Cleavage of structural proteins during the assembly of the head of bacteriophage T4.在噬菌体T4头部组装过程中结构蛋白的切割
Nature. 1970 Aug 15;227(5259):680-5. doi: 10.1038/227680a0.
9
Isolation of H-2 alloantigens solubilized by the detergent NP-40.通过去污剂NP - 40溶解的H - 2同种抗原的分离。
J Immunol. 1971 Nov;107(5):1363-7.
10
Isolation of glycoproteins from pig lymphocyte plasma membrane using Lens culinaris phytohemagglutinin.利用菜豆凝集素从猪淋巴细胞质膜中分离糖蛋白。
Biochem Biophys Res Commun. 1972 May 26;47(4):923-30. doi: 10.1016/0006-291x(72)90581-5.