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1
Genetic control of cell-mediated responsiveness to an AKR tumor-associated antigen: mapping of the locus involved to the I region of the H-2 complex.细胞介导的对AKR肿瘤相关抗原反应性的遗传控制：将相关基因座定位到H-2复合体的I区
J Exp Med. 1977 Nov 1;146(5):1367-79. doi: 10.1084/jem.146.5.1367.
2
Genetic control of the induction of cytolytic T lymphocyte responses to AKR/Gross viral leukemias. II. Negative control by the Fv-1 locus in AKR mice of responder H-2b haplotype.对AKR/Gross病毒性白血病细胞毒性T淋巴细胞反应诱导的遗传控制。II. 应答性H-2b单倍型AKR小鼠中Fv-1基因座的负调控。
J Immunol. 1984 May;132(5):2665-71.
3
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.
4
Modulation of F1 cytotoxic potentials by graft-vs-host reaction. Cooperative non-H-2- and H-2D region-gene control of F1 natural resistance to graft-vs-host reaction-associated immunosuppression.移植物抗宿主反应对F1细胞毒性潜能的调节。F1对移植物抗宿主反应相关免疫抑制的天然抗性的非H-2和H-2D区域基因协同控制。
J Immunol. 1989 Mar 1;142(5):1495-9.
5
Cell-mediated anti-tumor response in the RLmale 1 system. II. Control of the T killer cells by an H-2-linked Ir gene interfering with non-H-2 factors.RLmale 1系统中的细胞介导抗肿瘤反应。II. 由一个与H-2连锁的Ir基因干扰非H-2因子对T杀伤细胞的控制。
Eur J Immunol. 1980 Jan;10(1):26-30. doi: 10.1002/eji.1830100106.
6
Leukemogenesis, immune responsiveness, and murine leukemia virus expression in congenic AKR/J mice differing at H-2.在H-2位点存在差异的同源AKR/J小鼠中的白血病发生、免疫反应性及小鼠白血病病毒表达
Infect Immun. 1980 Sep;29(3):1007-12. doi: 10.1128/iai.29.3.1007-1012.1980.
7
Variation in MHC antigenic profiles of tumor cells and its biological effects.肿瘤细胞MHC抗原谱的变化及其生物学效应。
Immunol Rev. 1981;60:85-127. doi: 10.1111/j.1600-065x.1981.tb00363.x.
8
AKR/J gene(s) unlinked to H-2 determines dominant inheritance of lymphocyte hyporesponsiveness to acetylcholine receptor.与H-2不连锁的AKR/J基因决定淋巴细胞对乙酰胆碱受体低反应性的显性遗传。
J Immunol. 1985 Apr;134(4):2079-83.
9
In vivo or in vitro treatments with anti-I-J alloantisera abolish immunity to AKR leukemia.用抗I-J同种异体抗血清进行体内或体外处理可消除对AKR白血病的免疫。
Proc Natl Acad Sci U S A. 1980 Apr;77(4):2178-82. doi: 10.1073/pnas.77.4.2178.
10
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.

引用本文的文献

1
I-region linked complementing loci in resistance to viral leukemogenesis in the mouse.I 区连接的互补基因座在小鼠抗病毒白血病发生中的作用。
Immunogenetics. 1980;10(6):535-43. doi: 10.1007/BF01572588.
2
Genetic control of responsiveness to the tumor-associated transplantation antigen of a chemically induced murine fibrosarcoma.化学诱导的小鼠纤维肉瘤的肿瘤相关移植抗原反应性的遗传控制。
Immunogenetics. 1978 Dec;7(1):271-5. doi: 10.1007/BF01844015.
3
In vivo or in vitro treatments with anti-I-J alloantisera abolish immunity to AKR leukemia.用抗I-J同种异体抗血清进行体内或体外处理可消除对AKR白血病的免疫。
Proc Natl Acad Sci U S A. 1980 Apr;77(4):2178-82. doi: 10.1073/pnas.77.4.2178.
4
Role of the major histocompatibility complex in resistance to viral leukemia; its effect on the preleukemic stage of leukemogenesis.主要组织相容性复合体在抵抗病毒性白血病中的作用；其对白血病发生前期的影响。
Springer Semin Immunopathol. 1982;4(4):373-96. doi: 10.1007/BF02053740.
5
H-21-linked control of immunological resistance to viral leukemogenesis as a response to preleukemic cells.作为对白血病前期细胞的一种反应，H-21连锁的对病毒性白血病发生的免疫抗性控制。
Immunogenetics. 1981 Mar 1;12(5-6):423-32. doi: 10.1007/BF01561685.
6
I-J restrictions on the activation and interaction of parental and F1-derived TS3 suppressor cells.亲本和F1衍生的TS3抑制细胞激活与相互作用的I-J限制
J Exp Med. 1982 Aug 1;156(2):465-79. doi: 10.1084/jem.156.2.465.
7
Influence of the major histocompatibility complex on the repertoire of allospecific cytolytic T lymphocytes.主要组织相容性复合体对同种特异性细胞溶解T淋巴细胞库的影响。
J Exp Med. 1982 Feb 1;155(2):380-9. doi: 10.1084/jem.155.2.380.
8
HLA and adult T cell leukaemia: HLA-linked genes controlling susceptibility to human T cell leukaemia virus type I.人类白细胞抗原与成人T细胞白血病：控制对I型人类T细胞白血病病毒易感性的人类白细胞抗原连锁基因。
Clin Exp Immunol. 1988 Feb;71(2):211-6.
9
A role for elevated H-2 antigen expression in resistance to neoplasia caused by radiation-induced leukemia virus. Enhancement of effective tumor surveillance by killer lymphocytes.H-2抗原表达升高在抵抗辐射诱导的白血病病毒所致肿瘤形成中的作用。杀伤淋巴细胞增强有效的肿瘤监测。
J Exp Med. 1979 Apr 1;149(4):898-909. doi: 10.1084/jem.149.4.898.
10
The generation and specificity of cytotoxic T cells raised against syngeneic tumor cells bearing AKR/Gross murine leukemia virus antigens.针对携带AKR/Gross小鼠白血病病毒抗原的同基因肿瘤细胞产生的细胞毒性T细胞的生成及特异性。
J Exp Med. 1979 Jul 1;150(1):51-66. doi: 10.1084/jem.150.1.51.

本文引用的文献

1
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.
2
Occurrence of natural antibody to the G (gross) leukemia antigen in mice.小鼠中针对G（总）白血病抗原的天然抗体的出现。
Cancer Res. 1966 Jul;26(7):1415-9.
3
The effect of histocompatibility-2 type on response to friend leukemia virus in mice.组织相容性-2类型对小鼠对Friend白血病病毒反应的影响。
J Exp Med. 1968 Mar 1;127(3):465-73. doi: 10.1084/jem.127.3.465.
4
Leukemia-associated transplantation antigens related to murine leukemia virus. The X.1 system: immune response controlled by a locus linked to H-2.与鼠白血病病毒相关的白血病相关移植抗原。X.1系统：由与H-2连锁的基因座控制的免疫反应。
J Exp Med. 1973 Sep 1;138(3):593-606. doi: 10.1084/jem.138.3.593.
5
Histocompatibility-linked genetic control of disease susceptibility. Murine lymphocytic choriomeningitis virus infection.疾病易感性的组织相容性连锁基因控制。小鼠淋巴细胞性脉络丛脑膜炎病毒感染。
J Exp Med. 1973 May 1;137(5):1201-12. doi: 10.1084/jem.137.5.1201.
6
Protein clinical manifestations of primary tumors of the heart.心脏原发性肿瘤的蛋白质临床表现。
Am J Med. 1972 Jan;52(1):1-8. doi: 10.1016/0002-9343(72)90002-2.
7
Host genetic control of recovery from Friend leukemia virus-induced splenomegaly: mapping of a gene within the major histocompatability complex.宿主对弗氏白血病病毒诱导的脾肿大恢复的遗传控制：主要组织相容性复合体内一个基因的定位
J Exp Med. 1974 Dec 1;140(6):1457-67. doi: 10.1084/jem.140.6.1457.
8
The H-2 locus and viral leukemogenesis as studied in congenic strains of mice.在小鼠同源近交系中研究的H-2基因座与病毒性白血病发生
J Natl Cancer Inst. 1968 Aug;41(2):597-604.
9
The role of genetics in Gross virus leukemogenesis.遗传学在格罗斯病毒白血病发生中的作用。
Bibl Haematol. 1970(36):213-20. doi: 10.1159/000391710.
10
Genetic control of immune responses in vitro. V. Stimulation of suppressor T cells in nonresponder mice by the terpolymer L-glutamic acid 60-L-alanine 30-L-tyrosine 10 (GAT).体外免疫反应的遗传控制。V. 三元共聚物L-谷氨酸60-L-丙氨酸30-L-酪氨酸10（GAT）对无反应小鼠中抑制性T细胞的刺激
J Exp Med. 1974 Sep 1;140(3):648-59. doi: 10.1084/jem.140.3.648.

细胞介导的对AKR肿瘤相关抗原反应性的遗传控制：将相关基因座定位到H-2复合体的I区

Genetic control of cell-mediated responsiveness to an AKR tumor-associated antigen: mapping of the locus involved to the I region of the H-2 complex.

作者信息

Meruelo D, Deak B, McDevitt H O

出版信息

J Exp Med. 1977 Nov 1;146(5):1367-79. doi: 10.1084/jem.146.5.1367.

DOI:10.1084/jem.146.5.1367
PMID:411874
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2180965/
Abstract

The role of H-2-linked genes in controlling resistance to murine leukemia viruses has been studied by measuring the cell-mediated immune response of F1 hybrid mice (between AKR and various C3H and C57BL/10 derived, H-2 congenic strains) to an AKR tumor cell line, BW5147. The studies have shown that the ability to generate a primary or secondary cell-mediated response to an AKR tumor cell antigenic determinant is under H-2 linked control. The locus determining CML responsiveness maps in the I-J subregion. Nonresponsiveness is associated with the H-2q/k and H-2b/k hybrid genotypes, whereas responsiveness is associated with the H-2k/k homozygous genotype. Nonresponsiveness may result from (a) dominant suppression; (b) recessive responsiveness; or (c) an alternate mechanism not yet understood. This type of control may be one of several H-2-associated mechanisms of defense against virus-induced neoplasms.

摘要

通过测量F1杂种小鼠（AKR与各种源自C3H和C57BL/10的H-2同源品系之间）对AKR肿瘤细胞系BW5147的细胞介导免疫反应，研究了H-2连锁基因在控制对鼠白血病病毒抗性中的作用。研究表明，对AKR肿瘤细胞抗原决定簇产生初次或二次细胞介导反应的能力受H-2连锁控制。决定CML反应性的基因座定位于I-J亚区。无反应性与H-2q/k和H-2b/k杂种基因型相关，而反应性与H-2k/k纯合基因型相关。无反应性可能是由于（a）显性抑制；（b）隐性反应性；或（c）一种尚未理解的替代机制。这种控制类型可能是几种与H-2相关的抗病毒诱导肿瘤防御机制之一。