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Evaluation of the toxicity of iron-ion irradiation in murine bone marrow dendritic cells via increasing the expression of indoleamine 2,3-dioxygenase 1

文献类型：期刊论文

作者Xie, Yi1,2,3; Yan, Jun-Fang1,2,3,4; Ma, Jing-Yi5; Li, Hong-Yan1,2,3; Ye, Yan-Cheng6; Zhang, Yan-Shan6; Zhang, Hong1,2,3,6
刊名TOXICOLOGY RESEARCH
出版日期2017-11-01
卷号6页码:958-968
ISSN号2045-452X
DOI10.1039/c7tx00194k
英文摘要High linear energy transfer radiation is known to deposit higher energy in tissues and cause greater toxicity compared to low-LET irradiation. Local immunosuppression is frequently observed after irradiation (IR). Dendritic cells (DCs) play important roles in the initiation and maintenance of the immune response. The dysfunction of DCs contributes to tumor evasion and growth. However, molecular mechanisms underlying the establishment of immune tolerance induced by heavy ion IR through this DC population are poorly understood. Therefore, here we report our findings on the dysfunction of bone marrow-derived dendritic cells (BMDCs) induced by 1 Gy iron ion radiation and promotions of expressions of JNK1/2/3, indoleamine 2,3-dioxygenase 1 (IDO1), p-ERK1/2 and p38/MAPK; and decrease of IDO2, MHC class II, CD40, CD80 expressions and IFN-gamma and TNF-alpha secretion after total-body IR in mice. JNK(+) IDO1(+) BMDCs showed up-expression of p-ERK1/2 and p-p38/MAPK, reduced expression of MHC class II and CD80, and were not able to effectively stimulate allogeneic spleen T cells. The inhibition of IDO1 expressions could partly restore the function of BMDCs. In all, our study shows that elevated JNK and IDO1 expression induced by Fe ion IR could result in dysfunction of BMDCs via p-p38/MAPK and p-ERK1/2 signal pathway, and it may represent a new mechanism in radiation-induced immune tolerance.
WOS关键词T-CELLS ; TRYPTOPHAN CATABOLISM ; SIGNALING PATHWAYS ; TOLERANCE ; MAPK ; PROLIFERATION ; MOLECULES ; APOPTOSIS ; RESPONSES ; KINASE
资助项目National Natural Science Foundation of China[U1432248] ; National Natural Science Foundation of China[11605260] ; Ministry of Science and Technology[2016YFC0904602] ; Chinese Academy of Sciences
WOS研究方向Toxicology
语种英语
出版者ROYAL SOC CHEMISTRY
WOS记录号WOS:000413929700019
资助机构National Natural Science Foundation of China ; Ministry of Science and Technology ; Chinese Academy of Sciences
源URL[http://119.78.100.186/handle/113462/46031]  
专题中国科学院近代物理研究所
通讯作者Zhang, Hong
作者单位1.Chinese Acad Sci, Inst Modern Phys, 509 Nanchang Rd, Lanzhou 730000, Gansu, Peoples R China
2.Inst Modern Phys, CAS Key Lab Heavy Ion Radiat Biol & Med, Lanzhou 730000, Gansu, Peoples R China
3.Key Lab Basic Res Heavy Ion Radiat Applicat Med, Lanzhou 730000, Gansu, Peoples R China
4.Univ Chinese Acad Sci, Grad Sch, Beijing 100039, Peoples R China
5.Sun Yat Sen Univ, Sch Pharmaceut Sci, Guangzhou 510006, Guangdong, Peoples R China
6.Gansu Wuwei Tumor Hosp, Wuwei 733000, Peoples R China
推荐引用方式
GB/T 7714		 Xie, Yi,Yan, Jun-Fang,Ma, Jing-Yi,et al. Evaluation of the toxicity of iron-ion irradiation in murine bone marrow dendritic cells via increasing the expression of indoleamine 2,3-dioxygenase 1[J]. TOXICOLOGY RESEARCH,2017,6:958-968.
APA Xie, Yi.,Yan, Jun-Fang.,Ma, Jing-Yi.,Li, Hong-Yan.,Ye, Yan-Cheng.,...&Zhang, Hong.(2017).Evaluation of the toxicity of iron-ion irradiation in murine bone marrow dendritic cells via increasing the expression of indoleamine 2,3-dioxygenase 1.TOXICOLOGY RESEARCH,6,958-968.
MLA Xie, Yi,et al."Evaluation of the toxicity of iron-ion irradiation in murine bone marrow dendritic cells via increasing the expression of indoleamine 2,3-dioxygenase 1".TOXICOLOGY RESEARCH 6(2017):958-968.

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来源：近代物理研究所

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