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从弗瑞德氏逆转录病毒诱导的白血病中自发恢复。Rfv-2基因在小鼠主要组织相容性复合体Q/TL区域的定位。

Spontaneous recovery from Friend retrovirus-induced leukemia. Mapping of the Rfv-2 gene in the Q/TL region of mouse MHC.

作者信息

Miyazawa M, Nishio J, Wehrly K, David C S, Chesebro B

机构信息

Laboratory of Persistent Viral Diseases, National Institutes of Health, National Institute of Allergy and Infections Diseases, Hamilton, MT 59840.

出版信息

J Immunol. 1992 Mar 15;148(6):1964-7.

PMID:1541833
Abstract

The Rfv-2 gene that influences the rate of spontaneous recovery from erythroleukemia induced by a low dose of Friend retrovirus complex was mapped to the Q/TL region of mouse MHC. Rfv-2 was physically and functionally distinct from the I-A-linked Ir gene that has been shown to control the responsiveness of Th cells to the envelope glycoprotein of Friend murine leukemia helper virus. The negative effect of the Rfv-2s allele was overcome by the B10.D2-H-2dm1 mutation of the D-L genes of H-2, suggesting functional similarities between the D-L and Q/TL genes in influencing resistance against Friend murine leukemia retrovirus complex infection or possible modification of Q/TL expression by genes in the D-L region.

摘要

影响低剂量Friend逆转录病毒复合物诱导的红白血病自发恢复率的Rfv-2基因被定位到小鼠MHC的Q/TL区域。Rfv-2在物理和功能上与I-A连锁的Ir基因不同,后者已被证明可控制Th细胞对Friend鼠白血病辅助病毒包膜糖蛋白的反应性。H-2的D-L基因的B10.D2-H-2dm1突变克服了Rfv-2s等位基因的负面影响,这表明D-L和Q/TL基因在影响对Friend鼠白血病逆转录病毒复合物感染的抗性方面具有功能相似性,或者D-L区域的基因可能对Q/TL表达进行修饰。

相似文献

1
Spontaneous recovery from Friend retrovirus-induced leukemia. Mapping of the Rfv-2 gene in the Q/TL region of mouse MHC.从弗瑞德氏逆转录病毒诱导的白血病中自发恢复。Rfv-2基因在小鼠主要组织相容性复合体Q/TL区域的定位。
J Immunol. 1992 Mar 15;148(6):1964-7.
2
Influence of MHC genes on spontaneous recovery from Friend retrovirus-induced leukemia.MHC基因对Friend逆转录病毒诱导的白血病自然恢复的影响。
J Immunol. 1992 Jan 15;148(2):644-7.
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Rfv-1 and Rfv-2, two H-2-associated genes that influence recovery from Friend leukemia virus-induced splenomegaly.Rfv-1和Rfv-2,两个与H-2相关的基因,它们影响从弗氏白血病病毒诱导的脾肿大中恢复。
J Immunol. 1978 Apr;120(4):1081-5.
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Different H-2 subregions influence immunization against retrovirus and immunosuppression.不同的H-2亚区影响针对逆转录病毒的免疫接种和免疫抑制。
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Identification of a non-H-2 gene (Rfv-3) influencing recovery from viremia and leukemia induced by Friend virus complex.鉴定一种影响从弗氏病毒复合物诱导的病毒血症和白血病中恢复的非H-2基因(Rfv-3)。
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H-2-associated and background genes influence the development of a murine retrovirus-induced immunodeficiency syndrome.H-2相关基因和背景基因影响小鼠逆转录病毒诱导的免疫缺陷综合征的发展。
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Detailed mapping of the Rfv-1 gene that influences spontaneous recovery from Friend retrovirus-induced leukaemia.对影响从Friend逆转录病毒诱导的白血病中自发恢复的Rfv-1基因进行详细定位。
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Host genetic factors that control immune responses to retrovirus infections.控制对逆转录病毒感染免疫反应的宿主遗传因素。
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Immunization with a single T helper cell epitope abrogates Friend virus-induced early erythroid proliferation and prevents late leukemia development.用单个辅助性T细胞表位进行免疫可消除弗氏病毒诱导的早期红系增殖,并预防晚期白血病的发生。
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Genetic control of T cell responsiveness to the Friend murine leukemia virus envelope antigen. Identification of class II loci of the H-2 as immune response genes.T细胞对弗氏鼠白血病病毒包膜抗原反应性的遗传控制。将H-2的Ⅱ类基因座鉴定为免疫反应基因。
J Exp Med. 1988 Nov 1;168(5):1587-605. doi: 10.1084/jem.168.5.1587.

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