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低剂量全身照射治愈小鼠因Friend病毒诱导的血液系统疾病:涉及γ干扰素和白细胞介素-2的可能机制

Cure with low-dose total-body irradiation of the hematological disorder induced in mice with the Friend virus: possible mechanism involving interferon-gamma and interleukin-2.

作者信息

Shen R N, Lu L, Feng G S, Miller J, Taylor M W, Broxmeyer H E

机构信息

Department of Medicine (Hematology/Oncology), Indiana University School of Medicine, Indianapolis 46202.

出版信息

Lymphokine Cytokine Res. 1991 Apr;10(1-2):105-9.

PMID:1908321
Abstract

The effects of split low-dose total-body irradiation (TBI; 150 cGy) on production of interferon (IFN)-gamma and Interleukin-2 (IL-2) and on the growth characteristics of erythroid progenitor cells (BFU-E) have been assessed in normal mice, normal mice receiving TBI only, mice infected with the polycythemia-inducing strain of the Friend virus complex (FVC-P), and FVC-P infected mice receiving 150 cGy TBI on days 5 and 12. It was found that lymphocytes from the spleens of TBI-treated mice previously infected with FVC-P produced in response to phytohemagglutinin (PHA) and concanavalin A (Con A) stimulation up to 15 times greater amounts of IFN-gamma than cells from untreated FVC-P-infected mice. IL-2 production in Con A-stimulated spleen cell cultures also increased when cells were isolated from FVC-P-infected mice treated by low-dose TBI compared to untreated FVC-P-infected mice. TBI treatment was associated with greater than 99% ablation of "erythropoietin-independent" BFU-E colony formation. The results suggest that the cure of FVC-P-infected mice by low-dose TBI may result from activation of the IFN-gamma system and IL-2 production.

摘要

在正常小鼠、仅接受全身照射(TBI)的正常小鼠、感染了Friend病毒复合体诱导多血症毒株(FVC-P)的小鼠以及在第5天和第12天接受150 cGy TBI的FVC-P感染小鼠中,评估了分次低剂量全身照射(150 cGy)对干扰素(IFN)-γ和白细胞介素-2(IL-2)产生以及对红系祖细胞(BFU-E)生长特性的影响。结果发现,先前感染FVC-P的经TBI处理小鼠脾脏中的淋巴细胞,在受到植物血凝素(PHA)和刀豆蛋白A(Con A)刺激后,产生的IFN-γ量比未处理的FVC-P感染小鼠的细胞多15倍。与未处理的FVC-P感染小鼠相比,当从经低剂量TBI处理的FVC-P感染小鼠中分离细胞时,Con A刺激的脾细胞培养物中IL-2的产生也增加。TBI治疗与超过99%的“不依赖促红细胞生成素”BFU-E集落形成的消融有关。结果表明,低剂量TBI治愈FVC-P感染小鼠可能是由于IFN-γ系统的激活和IL-2的产生。

相似文献

1
Cure with low-dose total-body irradiation of the hematological disorder induced in mice with the Friend virus: possible mechanism involving interferon-gamma and interleukin-2.低剂量全身照射治愈小鼠因Friend病毒诱导的血液系统疾病:涉及γ干扰素和白细胞介素-2的可能机制
Lymphokine Cytokine Res. 1991 Apr;10(1-2):105-9.
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Curative effect of split low dosage total-body irradiation on mice infected with the polycythemia-inducing strain of the Friend virus complex.分割低剂量全身照射对感染弗氏病毒复合体红细胞增多诱导株小鼠的疗效
Cancer Res. 1988 May 1;48(9):2399-403.
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Effect of split low dose total body irradiation on SFFV mRNA, genomic DNA and protein expression in mice infected with the Friend virus complex.低剂量分次全身照射对感染弗氏病毒复合物小鼠中SFFV mRNA、基因组DNA和蛋白表达的影响。
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Curative effect of split low dosage total-body irradiation on murine AIDS induced by Friend virus: the results and the possible mechanism.低剂量分次全身照射对Friend病毒诱导的小鼠艾滋病的疗效:结果与可能机制
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Synergistic effect of human lactoferrin and recombinant murine interferon-gamma on disease progression in mice infected with the polycythemia-inducing strain of the Friend virus complex.人乳铁蛋白与重组鼠γ干扰素对感染弗氏病毒复合体红细胞增多诱导株小鼠疾病进展的协同作用
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Protective influence of lactoferrin on mice infected with the polycythemia-inducing strain of Friend virus complex.乳铁蛋白对感染弗氏病毒复合体红细胞增多症诱导株的小鼠的保护作用。
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Efficacy of recombinant human macrophage colony-stimulating factor in combination with whole-body hyperthermia in the treatment of mice infected with the polycythemia-inducing strain of the Friend virus complex.重组人巨噬细胞集落刺激因子联合全身热疗治疗感染弗氏病毒复合体红细胞增多诱导株小鼠的疗效
Exp Hematol. 1991 Sep;19(8):804-9.
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Expression of Friend leukemia virus and spleen focus-forming virus-specific sequences in erythroid bursts and granulocyte-macrophage colonies from spleen and marrow of mice infected with Friend leukemia virus.感染弗氏白血病病毒的小鼠脾脏和骨髓中红系爆式集落及粒-巨噬细胞集落中弗氏白血病病毒和脾集落形成病毒特异性序列的表达
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Incapacity of hematopoietic stem cell-deprived mice to produce tumor colonies induced by Friend virus-infected cells.造血干细胞缺失的小鼠无法产生由感染Friend病毒的细胞诱导形成的肿瘤集落。
Exp Hematol. 1978 Nov;6(10):777-84.
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Interferon-gamma induction by lipopolysaccharide: dependence on interleukin 2 and macrophages.脂多糖诱导的γ干扰素:依赖于白细胞介素2和巨噬细胞。
J Immunol. 1986 Feb 1;136(3):963-70.

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