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小鼠暴露于伽马射线对Th1和Th2淋巴细胞相互作用的影响。

Effect of murine exposure to gamma rays on the interplay between Th1 and Th2 lymphocytes.

作者信息

Ghazy Amany A, Abu El-Nazar Salma Y, Ghoneim Hossam E, Taha Abdul-Rahman M, Abouelella Amira M

机构信息

Department of Immunology, Medical Research Institute, Alexandria University Alexandria, Egypt.

Department of Medical Biophysics, Medical Research Institute, Alexandria University Alexandria, Egypt.

出版信息

Front Pharmacol. 2015 Apr 9;6:74. doi: 10.3389/fphar.2015.00074. eCollection 2015.

DOI:10.3389/fphar.2015.00074
PMID:25914644
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4391034/
Abstract

Gamma radiation radiotherapy is one of the widely used treatments for cancer. There is an accumulating evidence that adaptive immunity is significantly contributes to the efficacy of radiotherapy. This study is carried out to investigate the effect of gamma rays on the interplay between Th1/Th2 response, splenocyte lymphoproliferative response to polyclonal mitogenic activators and lymphocytic capacity to produce IL-12 and IL-10 in mice. Results showed that exposure of intact spleens to different doses of γ-rays (5, 10, 20 Gy) caused spontaneous and dose-dependent immune stimulation manifested by enhanced cell proliferation and elevated IL-12 production with decreased IL-10 release (i.e., Th1 bias). While exposure of splenocytes suspension to different doses of γ-rays (5, 10, 20 Gy) showed activation in splenocytes stimulated by PWM at 5 Gy then a state of conventional immune suppression that is characterized by being dose-dependent and is manifested by decreased cell proliferation and IL-12 release accompanied by increase in IL-10 production (i.e., Th2 bias). In addition, we investigated the exposure of whole murine bodies to different doses of γ-rays and found that the exposure to low dose γ-rays (0.2 Gy) caused a state of immune stimulation terminated by a remarkable tendency for immune suppression. Exposure to 5 or 10 Gy of γ-rays resulted in a state of immune stimulation (Th1 bias), but exposure to 20 Gy showed a standard state of immune suppression (Th2 bias). The results indicated that apparently we can control the immune response by controlling the dose of γ-rays.

摘要

伽马辐射放疗是癌症广泛使用的治疗方法之一。越来越多的证据表明适应性免疫对放疗疗效有显著贡献。本研究旨在探讨伽马射线对小鼠Th1/Th2反应、脾细胞对多克隆有丝分裂原激活剂的淋巴细胞增殖反应以及产生IL-12和IL-10的淋巴细胞能力之间相互作用的影响。结果显示,完整脾脏暴露于不同剂量的γ射线(5、10、20 Gy)会引起自发的、剂量依赖性的免疫刺激,表现为细胞增殖增强、IL-12产生增加以及IL-10释放减少(即Th1偏向)。而脾细胞悬液暴露于不同剂量的γ射线(5、10、20 Gy)时,在5 Gy时经PWM刺激的脾细胞表现出激活,然后是一种典型的免疫抑制状态,其特征是剂量依赖性,表现为细胞增殖和IL-12释放减少,同时IL-10产生增加(即Th2偏向)。此外,我们研究了整个小鼠身体暴露于不同剂量γ射线的情况,发现低剂量γ射线(0.2 Gy)暴露会引起免疫刺激状态,随后显著倾向于免疫抑制。暴露于5或10 Gy的γ射线会导致免疫刺激状态(Th1偏向),但暴露于20 Gy则表现出标准的免疫抑制状态(Th2偏向)。结果表明,显然我们可以通过控制γ射线剂量来控制免疫反应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7284/4391034/00fd77cafa48/fphar-06-00074-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7284/4391034/efbe77882694/fphar-06-00074-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7284/4391034/847b97c972c2/fphar-06-00074-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7284/4391034/5b552f7ea2dc/fphar-06-00074-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7284/4391034/2829bf903300/fphar-06-00074-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7284/4391034/ceb4cf66db93/fphar-06-00074-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7284/4391034/c13322ef966b/fphar-06-00074-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7284/4391034/738e96a1672f/fphar-06-00074-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7284/4391034/a5bb309a592c/fphar-06-00074-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7284/4391034/00fd77cafa48/fphar-06-00074-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7284/4391034/efbe77882694/fphar-06-00074-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7284/4391034/847b97c972c2/fphar-06-00074-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7284/4391034/5b552f7ea2dc/fphar-06-00074-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7284/4391034/2829bf903300/fphar-06-00074-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7284/4391034/ceb4cf66db93/fphar-06-00074-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7284/4391034/c13322ef966b/fphar-06-00074-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7284/4391034/738e96a1672f/fphar-06-00074-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7284/4391034/a5bb309a592c/fphar-06-00074-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7284/4391034/00fd77cafa48/fphar-06-00074-g009.jpg

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