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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。

H-2D control of recovery from Friend virus leukemia: H-2D region influences the kinetics of the T lymphocyte response to Friend virus.

作者信息

Britt W J, Chesebro B

出版信息

J Exp Med. 1983 Jun 1;157(6):1736-45. doi: 10.1084/jem.157.6.1736.

DOI:10.1084/jem.157.6.1736
PMID:6406638
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2187025/
Abstract

A Friend virus (FV)-specific T lymphocyte proliferation assay was used to compare the T lymphocyte responses of H-2 congenic mice that differed in their ability to recover from FV leukemia after inoculation of high virus doses. Gene(s) of the H-2D region influenced the kinetics of this response such that H-2Db/b homozygous mice were positive 6-8 d earlier than H-2Dd/b mice. This correlated with the Rfv-1, H-2D-linked influence on recovery from FV by these mice, and also appeared to explain the prominent effect of virus dose on recovery incidence. These findings were supported by the ability of passively transferred immune splenic T lymphocytes to induce recovery from leukemia at 6 d after FV inoculation, but not at 16 d. H-2a/a mice were found to be unresponsive in the FV-specific T lymphocyte proliferation assay. This effect mapped to the left of H-2D, possibly in the H-2I region, and may be an in vitro manifestation of the Rfv-2 gene. No evidence for nonspecific immunosuppression of the T lymphocyte response to concanavalin A was observed in any of the H-2 congenic F1 mice studied.

摘要

采用脾友病毒(FV)特异性T淋巴细胞增殖试验,比较了接种高剂量病毒后从FV白血病恢复能力不同的H-2同类系小鼠的T淋巴细胞反应。H-2D区域的基因影响了这种反应的动力学,使得H-2Db/b纯合小鼠比H-2Dd/b小鼠早6 - 8天呈阳性反应。这与Rfv-1(与H-2D连锁)对这些小鼠从FV感染中恢复的影响相关,并且似乎也解释了病毒剂量对恢复发生率的显著影响。这些发现得到了如下结果的支持:被动转移的免疫脾T淋巴细胞能够在FV接种后6天而非16天诱导白血病恢复。在FV特异性T淋巴细胞增殖试验中,发现H-2a/a小鼠无反应。这种效应定位于H-2D左侧,可能在H-2I区域,并且可能是Rfv-2基因的一种体外表现。在所研究的任何H-2同类系F1小鼠中,均未观察到对伴刀豆球蛋白A的T淋巴细胞反应存在非特异性免疫抑制作用的证据。

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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。
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本文引用的文献

1
Eradication of disseminated murine leukemia by chemoimmunotherapy with cyclophosphamide and adoptively transferred immune syngeneic Lyt-1+2- lymphocytes.用环磷酰胺进行化学免疫疗法并过继转移同基因Lyt-1+2-淋巴细胞根除播散性小鼠白血病
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Cytotoxic T lymphocyte recognition of gp70 on Friend virus-induced erythroleukemia cell clones.细胞毒性T淋巴细胞对Friend病毒诱导的红白血病细胞克隆上gp70的识别。
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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。
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Inability of mice to generate cytotoxic T lymphocytes to vesicular stomatitis virus restricted to H-2Kk or H-2Dk.小鼠无法产生针对局限于H-2Kk或H-2Dk的水疱性口炎病毒的细胞毒性T淋巴细胞。
J Immunol. 1981 Feb;126(2):446-51.
5
Spontaneous cessation of Friend murine leukemia virus production by leukemia cell line Y57: overgrowth by nonproducer cells.白血病细胞系Y57自发停止产生弗氏鼠白血病病毒:非产生病毒细胞过度生长。
J Natl Cancer Inst. 1980 May;64(5):1153-9.
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.
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Immunodepression by oncogenic viruses.致癌病毒引起的免疫抑制。
Prog Med Virol. 1972;14:1-35.
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A miniaturized mouse mixed leukocyte culture in serum-free and mouse serum supplemented media.一种在无血清和添加小鼠血清的培养基中的小型化小鼠混合白细胞培养。
J Immunol Methods. 1973 Oct;3(2):147-63. doi: 10.1016/0022-1759(73)90030-6.
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In vitro depression of cellular immunity by Friend virus leukemic spleen cells.弗瑞德病毒白血病脾细胞对细胞免疫的体外抑制作用
Cell Immunol. 1975 May;17(1):57-73. doi: 10.1016/s0008-8749(75)80006-2.
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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.