期刊文献+

宫颈癌组织中DCR3表达与外周血T细胞亚群的相关性研究 被引量:8

Correlation between DCR3 expression and T cell subgroups in peripheral blood of uterine cervical cancer
原文传递
导出
摘要 目的探讨宫颈癌组织中诱骗受体3(DCR3)表达与外周血T细胞亚群之间的相关性。方法免疫组织化学法检测宫颈上皮内瘤变(CIN)、宫颈癌(CC)及正常宫颈组织中DCR3表达情况,并检测宫颈癌组织中实质及间质内T细胞表面抗原CD3、CD4、CD8阳性细胞数量;应用流式细胞术分析患者外周血中CD3+、CD4+、CD8+T数量变化情况,分析研究宫颈癌组织中DCR3表达与患者外周血T细胞亚群之间的相关性。结果 DCR3表达强度与宫颈病变严重程度有关;宫颈癌患者外周血中T细胞数明显降低,且宫颈组织中DCR3表达与患者外周血中CD3+T、CD4+/CD8+呈负相关;宫颈癌变后实质内T细胞数明显减少,T细胞主要聚集于肿瘤间质内。结论 DCR3参与了宫颈癌细胞免疫逃逸,外周血T细胞亚群联合DCR3检测可作为宫颈癌免疫诊断指标,为患者免疫治疗提供基础。 To investigate the c orrelation between the expression of decoy receptor 3(DCR3) and T cell subgroup in peripheral blood of uterine cervical cancer patients, we detected the expression of DCR3 in cervical intraepithelial neoplasia(CIN), cervical cancer(CC) and normal cervical tissues. Furthermore, immunohistochemical method(IHC) and flow cytometry(FCM) were applied to detect the counts of CD3, CD4, and CD8 positive cells in parenchyma and mesenchymal, as well as in peripheral blood of cervical cancer patients. Data showed that the expression of DCR3 was related to the cervical lesion severity; the number of T cells were significantly lowered in peripheral blood of cervical cancer patients, and there was obvious negative correlation between DCR3 expression and CD3^+, CD4^+/CD8^+T in peripheral blood; the number of T cells were seriously reduced in the essence of cancer,and T cells mainly aggregated in the tumor stroma. Therefore, we presumed that DCR3 is related to tumor immune escape in patients with cervical cancer. And the expression and distribution of T cells in local tissues of cervical cancer can reflect the state of the body's immune function.
出处 《免疫学杂志》 CAS CSCD 北大核心 2015年第3期246-249,共4页 Immunological Journal
基金 湖北民族学院科技学院科研项目(KY201410) 湖北省教育厅科学技术研究项目(D20131904) 湖北民族学院科技学院大学生科技创新项目(K201307)
关键词 宫颈癌 DCR3 免疫逃逸 T细胞 Cervical cancer DCR3 Immune escape T cell
  • 相关文献

参考文献14

二级参考文献46

共引文献59

同被引文献75

  • 1谭诗生,李杭,罗健,陈南江,宋毅,姜桂林,杨飞月.欧洲癌症研究与治疗组织研制的生活质量核心调查问卷第3版中文版生活质量调查问卷测评[J].中国临床康复,2006,10(4):23-27. 被引量:312
  • 2Biteau B, Labarre J, Toledano MB. ATP-dependent reduction of cysteine-sulphinic acid by S. cerevisiae sulphiredoxin [J]. Nature, 2003, 425(6961): 980-984.
  • 3Hartikainen JM, Tengstrom M, Kosma VM, et al. Genetic polymorphisms and protein expression of NRF2 and Sulfiredoxin predict survival outcomes in breast cancer [J]. Cancer Res, 2012, 72(21): 5537-5546.
  • 4Wei Q, Jiang H, Xiao Z, et al. Sulfiredoxin-Peroxiredoxin IV axis promotes human lung cancer progression through modulation of specific phosphokinase signaling[J]. Proe Natl Acad Sei USA, 2011, 108(17): 7004-7009.
  • 5Gao Q, Liu W, Cai J, et al. EphB2 promotes cervical cancer progression by inducing epithelial--mesenchymal transition [J]. Hum Pathol, 2014, 45(2): 372-381.
  • 6Wang WS, Yu SL, Yang XS, et al. Expression and significance of twist and E-cadherin in ovarian cancer tissues[J]. Asian Pac J Cancer Pre, 2013, 14(2): 669-672.
  • 7Fulga V, Rudico L, Balica AR, et al. Differential expression of e-cadherin in primary breast cancer and corresponding lymph node metastases[J]. Anticancer Res, 2015, 35(2): 759-765.
  • 8Ha B, Kim EK, Kim JH, et al. Human peroxiredoxin 1 modulates TGF-betal-induced epithelial-mesenchymal transition through its peroxidase activity[J]. Biochem Biophys Res Commun, 2012, 421(1): 33-37.
  • 9Kwak MK, Wakabayashi N, Itoh K, et al. Modulation of gene expression by cancer chemopreventive dithiolethionesthrough the Keapl-Nrf2 pathway. Identification of novel gene clusters for cell survival[J]. J Biol Chem, 2003, 278(10): 8135-8145.
  • 10Wei Q, Jiang H, Baker A, et al. Loss of sulfiredoxin renders mice resistant to azoxymethane/dextran sulfate sodium- induced colon carcinogenesis[J]. Carcinogenesis, 2013, 34(6): 1403-1410.

引证文献8

二级引证文献50

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部