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辐射白血病病毒(RadLV)的高致白血病和低致白血病变体:与致白血病活性相关的免疫原性、抑制性和遗传特性

High- and low-leukemogenic variants of the radiation leukemia virus (RadLV): immunogenic, suppressive and genetic properties in relation to leukemogenic activity.

作者信息

Yefenof E, Ben David Y, Kotler M

出版信息

Int J Cancer. 1984 Dec 15;34(6):875-82. doi: 10.1002/ijc.2910340621.

DOI:10.1002/ijc.2910340621
PMID:6439654
Abstract

C57BL/6 (B6) mice inoculated with the highly leukemogenic variant of the radiation leukemia virus (A-RadLV) develop suppressor cells capable of abrogating potential anti-tumor immunity in vitro and in vivo. Inoculation of B6 animals with the low-leukemogenic D-RadLV variant does not result in suppressor cell generation but induces antitumor reactive lymphocytes. A-RadLV and D-RadLV are not leukemogenic in BALB/c or (B6 X BALB/c)F1(F1) mice, and reactive but not suppressor lymphocytes could be demonstrated in F1 animals inoculated with either virus. Infectivity assays and fingerprint analysis revealed that A-RadLV and D-RadLV contain viruses with N and B tropism. In addition, thymoma cells induced by A-RadLV produced another virus with a fingerprint pattern containing X-MuLV elements. The possible implications of the different virus types on the immunogenic and leukemogenic properties of the RadLV variants are discussed.

摘要

接种辐射白血病病毒(A-RadLV)高致白血病变体的C57BL/6(B6)小鼠会产生抑制细胞,这些抑制细胞在体外和体内均能消除潜在的抗肿瘤免疫。用低致白血病的D-RadLV变体接种B6动物不会导致抑制细胞的产生,但会诱导抗肿瘤反应性淋巴细胞。A-RadLV和D-RadLV在BALB/c或(B6×BALB/c)F1(F1)小鼠中不具有致白血病性,在用任何一种病毒接种的F1动物中都可证明存在反应性淋巴细胞而非抑制性淋巴细胞。感染性测定和指纹分析表明,A-RadLV和D-RadLV含有具有N和B嗜性的病毒。此外,由A-RadLV诱导的胸腺瘤细胞产生了另一种具有包含X-MuLV元件指纹图谱的病毒。本文讨论了不同病毒类型对RadLV变体免疫原性和致白血病性的可能影响。

相似文献

1
High- and low-leukemogenic variants of the radiation leukemia virus (RadLV): immunogenic, suppressive and genetic properties in relation to leukemogenic activity.辐射白血病病毒(RadLV)的高致白血病和低致白血病变体:与致白血病活性相关的免疫原性、抑制性和遗传特性
Int J Cancer. 1984 Dec 15;34(6):875-82. doi: 10.1002/ijc.2910340621.
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Immunity and suppression in radiation- and radiation leukemia virus (RadLV)-induced leukemogenesis.辐射及辐射白血病病毒(RadLV)诱导白血病发生过程中的免疫与抑制作用
Leuk Res. 1986;10(7):797-801. doi: 10.1016/0145-2126(86)90300-0.
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High- and low-leukemogenic variants of the radiation leukemia virus (RadLV) differ in ability to induce tumor-specific immune suppression.辐射白血病病毒(RadLV)的高致白血病和低致白血病变体在诱导肿瘤特异性免疫抑制的能力上存在差异。
Int J Cancer. 1982 Sep 15;30(3):355-9. doi: 10.1002/ijc.2910300316.
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Immunologic characteristics in relation to high and low leukemogenic activity of radiation leukemia virus variants. II. Analysis of the immune response.与辐射白血病病毒变种高低致白血病活性相关的免疫学特征。II. 免疫反应分析。
J Immunol. 1977 Feb;118(2):607-11.
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Immunologic characteristics in relation to high and low leukemogenic activity of radiation leukemia virus variants. I. Cellular analysis of immunosuppression.与辐射白血病病毒变异体高低致白血病活性相关的免疫学特征。I. 免疫抑制的细胞分析。
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A highly leukemogenic radiation leukemia virus isolate is a thymotropic, immunosuppressive retrovirus with a unique RNA structure.
Int J Cancer. 1987 Apr 15;39(4):492-7. doi: 10.1002/ijc.2910390415.
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Suppressor and reactive lymphocytes in radiation leukemia virus (RadLV)-induced leukemogenesis.辐射白血病病毒(RadLV)诱导白血病发生过程中的抑制性淋巴细胞和反应性淋巴细胞
Cancer Immunol Immunother. 1983;16(1):48-52. doi: 10.1007/BF00199905.
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In vitro generation of cytotoxic lymphocytes against radiation- and radiation leukemia virus-induced tumors. III. Suppression of anti-tumor immunity in vitro by lymphocytes of mice undergoing radiation leukemia virus-induced leukemogenesis.针对辐射及辐射白血病病毒诱导肿瘤的细胞毒性淋巴细胞的体外生成。III. 处于辐射白血病病毒诱导白血病发生过程中的小鼠淋巴细胞对体外抗肿瘤免疫的抑制作用。
J Exp Med. 1980 Dec 1;152(6):1473-83. doi: 10.1084/jem.152.6.1473.
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Molecular basis of a unique tumor antigen of radiation leukemia virus-induced leukemia B6RV2: its relation to MuLV gp70 of xenotropic class.
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Studies on emerging radiation leukemia virus variants in C57BL/Ka mice.C57BL/Ka小鼠中新兴辐射白血病病毒变体的研究。
J Virol. 1986 Apr;58(1):96-106. doi: 10.1128/JVI.58.1.96-106.1986.

引用本文的文献

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Potentiation of T cell immunity against radiation-leukemia-virus-induced lymphoma by polysaccharide K.多糖K增强T细胞对辐射白血病病毒诱导淋巴瘤的免疫作用。
Cancer Immunol Immunother. 1991;34(2):133-7. doi: 10.1007/BF01741348.