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FLD-3 弗氏红白血病细胞在体内外的裂解:89Sr 治疗和弗氏病毒感染的影响

Lysis of FLD-3 Friend erythroleukemia cells in vitro and in vivo: effect of 89Sr treatment and Friend virus infection.

作者信息

Lust J A, Bennett M, Kumar V

出版信息

Int J Cancer. 1984 Jan 15;33(1):107-13. doi: 10.1002/ijc.2910330117.

DOI:10.1002/ijc.2910330117
PMID:6582049
Abstract

The effector cells from non-immunized mice capable of lysing 51Cr-labelled FLD-3 BALB/c Friend virus-induced erythroleukemia cells in vitro and cells capable of clearing FLD-3 cells labelled with 5-iodo-2'-deoxyuridine-125I (125IdUrd) from the lungs in vivo were characterized and compared with natural killer (NK) cells reactive against YAC-I lymphoma cells. Unlike NK cells, the cells capable of lysing FLD-3 cells in vitro were insensitive to antibodies directed against NK-2.1 or Thy-1.2 antigens (plus complement) and to pretreatment of mice in vivo with silica particles, 89Sr or estradiol. Heat-killed C. parvum organism stimulated anti-FLD-3 effector cells without changing the slow rate (24 h) of lysis in vitro. The ability to clear FLD-3 and YAC-1 cells from the lung was normal and defective, respectively, in C57BL/6-bg/bg(beige) mice and in mice pretreated with 89Sr or estradiol. We conclude that natural cytotoxic (NC) cells lyse FLD-3 cells, Fv-2, which regulates resistance to leukemia induction by Friend virus, does not regulate NC(FLD-3) activity, and the virus does not affect NC(FLD-3) activity during the first several days of infection of normal genetically susceptible mice. However, infection of 89Sr-treated mice inhibits NC(FLD-3) function owing to the activation of suppressor cells. These data suggest (but do not prove) that effector cells similar or identical to NC(FLD-3) cells may function in vivo to resist the proliferation/survival of certain leukemia cells.

摘要

对来自未免疫小鼠的效应细胞进行了表征,这些细胞能够在体外裂解用51Cr标记的FLD - 3 BALB/c Friend病毒诱导的红白血病细胞,以及能够在体内清除肺部用5 - 碘 - 2'-脱氧尿苷 - 125I(125IdUrd)标记的FLD - 3细胞,并将其与对YAC - I淋巴瘤细胞有反应的自然杀伤(NK)细胞进行比较。与NK细胞不同,能够在体外裂解FLD - 3细胞的细胞对针对NK - 2.1或Thy - 1.2抗原(加补体)的抗体以及对小鼠体内用二氧化硅颗粒、89Sr或雌二醇进行的预处理不敏感。热灭活的微小隐孢子虫生物体刺激抗FLD - 3效应细胞,而不改变体外缓慢的裂解速率(24小时)。在C57BL/6 - bg/bg(米色)小鼠以及用89Sr或雌二醇预处理的小鼠中,从肺部清除FLD - 3和YAC - 1细胞的能力分别正常和有缺陷。我们得出结论,自然细胞毒性(NC)细胞裂解FLD - 3细胞,调节对Friend病毒诱导白血病抗性的Fv - 2不调节NC(FLD - 3)活性,并且在正常基因易感小鼠感染的最初几天,该病毒不影响NC(FLD - 3)活性。然而,89Sr处理小鼠的感染由于抑制细胞的激活而抑制NC(FLD - 3)功能。这些数据表明(但未证明)与NC(FLD - 3)细胞相似或相同的效应细胞可能在体内发挥作用以抵抗某些白血病细胞的增殖/存活。

相似文献

1
Lysis of FLD-3 Friend erythroleukemia cells in vitro and in vivo: effect of 89Sr treatment and Friend virus infection.FLD-3 弗氏红白血病细胞在体内外的裂解:89Sr 治疗和弗氏病毒感染的影响
Int J Cancer. 1984 Jan 15;33(1):107-13. doi: 10.1002/ijc.2910330117.
2
Natural immunity to grafts of FLD-3 erythroleukemia cells by irradiated mice.经辐照小鼠对FLD-3红白血病细胞移植的天然免疫
Nat Immun Cell Growth Regul. 1986;5(4):200-10.
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Lack of correlation between mycoplasma induced IFN-gamma production in vitro and natural killer cell activity against FLD-3 cells.
Immunobiology. 1983 Dec;165(5):445-58. doi: 10.1016/s0171-2985(83)80068-0.
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Mechanisms of genetic resistance to Friend virus leukemia in mice. II. Resistance of mitogen-responsive lymphocytes mediated by marrow-dependent cells.小鼠对弗氏病毒白血病的遗传抗性机制。II. 由骨髓依赖细胞介导的有丝分裂原反应性淋巴细胞的抗性
J Exp Med. 1976 Apr 1;143(4):713-27. doi: 10.1084/jem.143.4.713.
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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.
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Analysis of low natural killer cell activity in 89Sr-treated mice.对89锶处理小鼠低自然杀伤细胞活性的分析。
Eur J Immunol. 1982 May;12(5):442-5. doi: 10.1002/eji.1830120516.
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Hybrid resistance to EL-4 lymphoma cells. II. Association between loss of hybrid resistance and detection of suppressor cells after treatment of mice with 89Sr.对EL-4淋巴瘤细胞的杂种抗性。II. 用89Sr处理小鼠后杂种抗性丧失与抑制细胞检测之间的关联。
Scand J Immunol. 1981;13(6):563-71. doi: 10.1111/j.1365-3083.1981.tb00170.x.
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Hybrid resistance to EL-4 lymphoma cells. I. Characterization of natural killer cells that lyse EL-4 cells and their distinction from marrow-dependent natural killer cells.对EL-4淋巴瘤细胞的混合抗性。I. 裂解EL-4细胞的自然杀伤细胞的特性及其与骨髓依赖性自然杀伤细胞的区别。
J Exp Med. 1979 Sep 19;150(3):531-47. doi: 10.1084/jem.150.3.531.
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Macrophage-mediated natural cytotoxicity of dimethyl sulfoxide-treated Friend erythroleukemia cells.巨噬细胞介导的二甲基亚砜处理的弗氏红白血病细胞的天然细胞毒性。
J Natl Cancer Inst. 1985 Jul;75(1):105-10.
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Spontaneous regression of Friend murine leukemia virus-induced erythroleukemia. IV. Effects of radiation and athymia on leukemia regression in mice.弗瑞德氏鼠白血病病毒诱导的红细胞白血病的自然消退。IV. 辐射和无胸腺对小鼠白血病消退的影响。
J Natl Cancer Inst. 1979 Aug;63(2):449-54.

引用本文的文献

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Origin and differentiation of natural killer cells. III. Relationship between the precursors and effectors of natural killer and natural cytotoxic activity.自然杀伤细胞的起源与分化。III. 自然杀伤和自然细胞毒性活性的前体细胞与效应细胞之间的关系。
Immunol Res. 1986;5(1):16-24. doi: 10.1007/BF02917190.
2
Transplantable progenitors of natural killer cells are distinct from those of T and B lymphocytes.自然杀伤细胞的可移植祖细胞与T淋巴细胞和B淋巴细胞的可移植祖细胞不同。
Proc Natl Acad Sci U S A. 1986 May;83(10):3427-31. doi: 10.1073/pnas.83.10.3427.
3
Identification of a subset of murine natural killer cells that mediates rejection of Hh-1d but not Hh-1b bone marrow grafts.
鉴定出介导Hh-1d而非Hh-1b骨髓移植排斥反应的一小部分小鼠自然杀伤细胞。
J Exp Med. 1989 Jul 1;170(1):191-202. doi: 10.1084/jem.170.1.191.