H-2D（Rfv-1）基因对从弗氏病毒白血病中恢复的影响是由脾脏和骨髓的非白血病细胞介导的。
H-2D (Rfv-1) gene influence on recovery from Friend virus leukemia is mediated by nonleukemic cells of the spleen and bone marrow.
作者信息
Britt W J, Chesebro B
出版信息
J Exp Med. 1980 Dec 1;152(6):1795-804. doi: 10.1084/jem.152.6.1795.
Abstract
H-2D (Rfv-1)-associated control of recovery from FV leukemia was studied in congenic mice. In irradiation chimeras, the high recovery phenotype was transferred by cells of the spleen, bone marrow, and fetal liver. Furthermore, in cell transfers using unirradiated recipients, spleen and bone marrow cells of the high-recovery genotype were able to mediate recovery from leukemia in mice of the low-recovery genotype. Thus, the H-2D (Rfv-1) influence on recovery appeared to operate via nonleukemic cells of the spleen and bone marrow rather than via leukemic cells. The specific nonleukemic cell type(s) involved in recovery remains unknown. However, the mechanism appears to be complex and probably involves both anti-FV antibody and FV-specific cytotoxic T lymphocytes.
摘要
在同源小鼠中研究了H-2D（Rfv-1）相关的从FV白血病恢复的调控。在辐射嵌合体中，高恢复表型由脾脏、骨髓和胎肝细胞转移。此外，在使用未受辐射受体的细胞转移中，高恢复基因型的脾脏和骨髓细胞能够介导低恢复基因型小鼠从白血病中恢复。因此，H-2D（Rfv-1）对恢复的影响似乎是通过脾脏和骨髓的非白血病细胞而非白血病细胞起作用。参与恢复的具体非白血病细胞类型尚不清楚。然而，其机制似乎很复杂，可能涉及抗FV抗体和FV特异性细胞毒性T淋巴细胞。
相似文献
1
H-2D (Rfv-1) gene influence on recovery from Friend virus leukemia is mediated by nonleukemic cells of the spleen and bone marrow.H-2D（Rfv-1）基因对从弗氏病毒白血病中恢复的影响是由脾脏和骨髓的非白血病细胞介导的。
J Exp Med. 1980 Dec 1;152(6):1795-804. doi: 10.1084/jem.152.6.1795.
2
Anti-Friend virus antibody is associated with recovery from viremia and loss of viral leukemia cell-surface antigens in leukemic mice. Identification of Rfv-3 as a gene locus influencing antibody production.抗Friend病毒抗体与白血病小鼠病毒血症的恢复及病毒白血病细胞表面抗原的丧失有关。鉴定Rfv-3为影响抗体产生的基因座。
J Exp Med. 1979 Jul 1;150(1):10-9. doi: 10.1084/jem.150.1.10.
3
Immunosuppression by Friend leukemia virus is H-2 restricted by alloreactive T lymphocytes.弗氏白血病病毒引起的免疫抑制受同种异体反应性T淋巴细胞的H-2限制。
Proc Natl Acad Sci U S A. 1979 May;76(5):2415-9. doi: 10.1073/pnas.76.5.2415.
4
Antibody-induced loss of Friend virus leukemia cell surface antigens occurs during progression of erythroleukemia in F1 mice.在F1小鼠红白血病进展过程中，抗体诱导的Friend病毒白血病细胞表面抗原丢失发生。
J Exp Med. 1978 Nov 1;148(5):1109-21. doi: 10.1084/jem.148.5.1109.
5
6
Influence of the murine MHC (H-2) on Friend leukemia virus-induced immunosuppression.小鼠主要组织相容性复合体（H-2）对弗瑞德白血病病毒诱导的免疫抑制的影响。
J Exp Med. 1986 Feb 1;163(2):301-14. doi: 10.1084/jem.163.2.301.
7
Friend erythroleukemia antigen. A viral antigen specified by spleen focus-forming virus and differentiation antigen controlled by the Fv-2 locus.Friend红白血病抗原。一种由脾集落形成病毒指定的病毒抗原，以及受Fv-2基因座控制的分化抗原。
J Exp Med. 1979 May 1;149(5):1152-67. doi: 10.1084/jem.149.5.1152.
8
H-2D control of recovery from Friend virus leukemia: H-2D region influences the kinetics of the T lymphocyte response to Friend virus.H-2D对弗氏病毒白血病恢复的控制：H-2D区域影响T淋巴细胞对弗氏病毒反应的动力学。
J Exp Med. 1983 Jun 1;157(6):1736-45. doi: 10.1084/jem.157.6.1736.
9
New cell surface gp70 related to Friend mink cell focus-inducing virus is expressed on Friend virus-induced erythroleukemic spleen cells after elimination of ecotropic Friend virus gp70 in Rfv-3r/s mice.与弗氏水貂细胞灶诱导病毒相关的新细胞表面糖蛋白70，在Rfv-3r/s小鼠中消除嗜异性弗氏病毒糖蛋白70后，表达于弗氏病毒诱导的红白血病脾细胞上。
J Exp Med. 1981 Sep 1;154(3):868-82. doi: 10.1084/jem.154.3.868.
10
Antibody-induced modulation of Friend virus cell surface antigens decreases virus production by persistent erythroleukemia cells: influence of the Rfv-3 gene.抗体诱导的Friend病毒细胞表面抗原调节可降低持续性红白血病细胞的病毒产生：Rfv-3基因的影响。
Proc Natl Acad Sci U S A. 1979 Nov;76(11):5784-8. doi: 10.1073/pnas.76.11.5784.
引用本文的文献
1
Tetherin/BST-2: Restriction Factor or Immunomodulator?束缚素/BST-2：限制因子还是免疫调节剂？
Curr HIV Res. 2016;14(3):235-46. doi: 10.2174/1570162x14999160224102752.
2
Tetherin promotes the innate and adaptive cell-mediated immune response against retrovirus infection in vivo.Tetherin 促进了体内针对逆转录病毒感染的先天和适应性细胞介导的免疫反应。
J Immunol. 2014 Jul 1;193(1):306-16. doi: 10.4049/jimmunol.1400490. Epub 2014 May 28.
3
Major histocompatibility complex class I gene controls the generation of gamma interferon-producing CD4(+) and CD8(+) T cells important for recovery from friend retrovirus-induced leukemia.主要组织相容性复合体I类基因控制着对从Friend逆转录病毒诱导的白血病中恢复很重要的产生γ干扰素的CD4(+)和CD8(+) T细胞的生成。
J Virol. 2000 Jun;74(11):5363-7. doi: 10.1128/jvi.74.11.5363-5367.2000.
4
Recovery from Friend disease in mice with reduced major histocompatibility complex class I expression.主要组织相容性复合体I类表达降低的小鼠从Friend病中恢复。
J Virol. 1994 Apr;68(4):2059-64. doi: 10.1128/JVI.68.4.2059-2064.1994.
5
New cell surface gp70 related to Friend mink cell focus-inducing virus is expressed on Friend virus-induced erythroleukemic spleen cells after elimination of ecotropic Friend virus gp70 in Rfv-3r/s mice.与弗氏水貂细胞灶诱导病毒相关的新细胞表面糖蛋白70，在Rfv-3r/s小鼠中消除嗜异性弗氏病毒糖蛋白70后，表达于弗氏病毒诱导的红白血病脾细胞上。
J Exp Med. 1981 Sep 1;154(3):868-82. doi: 10.1084/jem.154.3.868.
6
H-2D control of recovery from Friend virus leukemia: H-2D region influences the kinetics of the T lymphocyte response to Friend virus.H-2D对弗氏病毒白血病恢复的控制：H-2D区域影响T淋巴细胞对弗氏病毒反应的动力学。
J Exp Med. 1983 Jun 1;157(6):1736-45. doi: 10.1084/jem.157.6.1736.
7
Identification of a unique erythroleukemia-associated retroviral gp70 expressed during early stages of normal erythroid differentiation.鉴定一种在正常红系分化早期表达的独特的红白血病相关逆转录病毒糖蛋白70。
J Exp Med. 1984 Jun 1;159(6):1591-603. doi: 10.1084/jem.159.6.1591.
本文引用的文献
1
HYBRID RESISTANCE CONTROLLED BY H-2 REGION: CORRECTION OF DATA.由H-2区域控制的杂种抗性：数据校正
Science. 1965 Feb 26;147(3661):1056. doi: 10.1126/science.147.3661.1056.
2
Immune response genes control T killer cell response against Moloney tumor antigen cytolysis regulating reactions against the best available H-2 + viral antigen association.免疫反应基因控制T杀伤细胞对莫洛尼肿瘤抗原的细胞溶解反应，调节针对最佳可用H-2+病毒抗原关联的反应。
J Exp Med. 1980 Jun 1;151(6):1468-76. doi: 10.1084/jem.151.6.1468.
3
Murine leukaemogenesis: monoclonal antibodies to T-cell determinants arrest T-lymphoma cell proliferation.小鼠白血病发生：针对T细胞决定簇的单克隆抗体可阻止T淋巴瘤细胞增殖。
Nature. 1980 May 22;285(5762):259-61. doi: 10.1038/285259a0.
4
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.
5
Cell transfer studies in a genetically controlled immune response.基因控制的免疫反应中的细胞转移研究。
Eur J Immunol. 1972 Jun;2(3):243-8. doi: 10.1002/eji.1830020310.
6
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.
7
Histocompatibility-linked immune response genes.组织相容性连锁免疫反应基因
Science. 1972 Jan 21;175(4019):273-9. doi: 10.1126/science.175.4019.273.
8
Studies on the role of the host immune response in recovery from Friend virus leukemia. I. Antiviral and antileukemia cell antibodies.宿主免疫反应在从弗氏病毒白血病恢复过程中的作用研究。I. 抗病毒和抗白血病细胞抗体。
J Exp Med. 1976 Jan 1;143(1):73-84. doi: 10.1084/jem.143.1.73.
9
Multiple H-2 linked immune response gene control of H-2 D-associated T-cell-mediated lympholysis to trinitrophenyl-modified autologous cells: Ir-like genes mapping to the left of I-A and within the I region.H-2 D相关的T细胞介导的对三硝基苯基修饰的自体细胞的淋巴细胞溶解的多个H-2连锁免疫反应基因控制：定位于I-A左侧和I区内的类Ir基因。
J Exp Med. 1976 Dec 1;144(6):1701-6. doi: 10.1084/jem.144.6.1701.
10
Mechanisms of genetic resistance to Friend virus leukemia. III. Susceptibility of mitogen-responsive lymphocytes mediated by T cells.对弗氏病毒白血病的遗传抗性机制。III. 由T细胞介导的有丝分裂原反应性淋巴细胞的易感性
J Exp Med. 1976 Apr 1;143(4):728-40. doi: 10.1084/jem.143.4.728.
Zotero 插件