[1] |
Arbyn M, Weiderpass E, Bruni L, et al. Estimates of incidence and mortality of cervical cancer in 2018: a worldwide analysis[J]. Lancet Glob Health, 2020, 8(2):e191-e203. doi: 10.1016/S2214-109X(19)30482-6.
doi: 10.1016/S2214-109X(19)30482-6
|
[2] |
Joharinia N, Farhadi A, Hosseini SY, et al. Association of HPV16 and 18 genomic copies with histological grades of cervical lesions[J]. Virusdisease, 2019, 30(3):387-393. doi: 10.1007/s13337-019-00545-2.
doi: 10.1007/s13337-019-00545-2
pmid: 31803806
|
[3] |
Gupta SM, Mania-Pramanik J. Molecular mechanisms in progression of HPV-associated cervical carcinogenesis[J]. J Biomed Sci, 2019, 26(1):28. doi: 10.1186/s12929-019-0520-2.
doi: 10.1186/s12929-019-0520-2
|
[4] |
范飞, 柳欣林, 李智海, 等. 人乳头瘤病毒衣壳蛋白结构生物学研究进展[J]. 中国生化药物杂志, 2016, 5:20-23,27. doi: 10.3969/j.issn.1005-1678.2016.05.06.
doi: 10.3969/j.issn.1005-1678.2016.05.06
|
[5] |
Ren S, Gaykalova DA, Guo T, et al. HPV E2, E4, E 5 drive alternative carcinogenic pathways in HPV positive cancers[J]. Oncogene, 2020, 39(40):6327-6339. doi: 10.1038/s41388-020-01431-8.
doi: 10.1038/s41388-020-01431-8
|
[6] |
Egawa N, Wang Q, Griffin HM, et al. HPV16 and 18 genome amplification show different E4-dependence, with 16E4 enhancing E1 nuclear accumulation and replicative efficiency via its cell cycle arrest and kinase activation functions[J]. PLoS Pathog, 2017, 13(3):e1006282. doi: 10.1371/journal.ppat.1006282.
doi: 10.1371/journal.ppat.1006282
|
[7] |
Li S, Hong X, Wei Z, et al. Ubiquitination of the HPV Oncoprotein E6 Is Critical for E6/E6AP-Mediated p53 Degradation[J]. Front Microbiol, 2019, 10:2483. doi: 10.3389/fmicb.2019.02483.
doi: 10.3389/fmicb.2019.02483
|
[8] |
Nogueira MO, Hošek T, Calçada EO, et al. Monitoring HPV-16 E7 phosphorylation events[J]. Virology, 2017, 503:70-75. doi: 10.1016/j.virol.2016.12.030.
doi: S0042-6822(16)30413-5
pmid: 28126639
|
[9] |
Smelov V, Elfström KM, Johansson AL, et al. Long-term HPV type-specific risks of high-grade cervical intraepithelial lesions: a 14-year follow-up of a randomized primary HPV screening trial[J]. Int J Cancer, 2015, 136(5):1171-1180. doi: 10.1002/ijc.29085.
doi: 10.1002/ijc.29085
|
[10] |
Doorbar J. Model systems of human papillomavirus-associated disease[J]. J Pathol, 2016, 238(2):166-179. doi: 10.1002/path.4656.
doi: 10.1002/path.4656
|
[11] |
Raikhy G, Woodby BL, Scott ML, et al. Suppression of Stromal Interferon Signaling by Human Papillomavirus 16[J]. J Virol, 2019, 93(19):e00458-19. doi: 10.1128/JVI.00458-19.
doi: 10.1128/JVI.00458-19
|
[12] |
Uppendahl LD, Dahl CM, Miller JS, et al. Natural Killer Cell-Based Immunotherapy in Gynecologic Malignancy: A Review[J]. Front Immunol, 2018, 8:1825. doi: 10.3389/fimmu.2017.01825.
doi: 10.3389/fimmu.2017.01825
|
[13] |
Stanley MA. Epithelial cell responses to infection with human papillomavirus[J]. Clin Microbiol Rev, 2012, 25(2):215-222. doi: 10.1128/CMR.05028-11.
doi: 10.1128/CMR.05028-11
|
[14] |
刘洪博, 王文智, 石庆芳. NK细胞和Treg细胞亚群在宫颈癌患者外周血中表达及临床意义[J]. 中国老年学杂志, 2020, 40(2):284-287. doi: 10.3969/j.issn.1005-9202.2020.02.018.
doi: 10.3969/j.issn.1005-9202.2020.02.018
|
[15] |
王玲. NK细胞对宫颈癌中免疫逃逸机制的影响[D]. 天津:天津医科大学, 2019.
|
[16] |
Miura S, Kawana K, Schust DJ, et al. CD1d, a sentinel molecule bridging innate and adaptive immunity, is downregulated by the human papillomavirus (HPV) E5 protein: a possible mechanism for immune evasion by HPV[J]. J Virol, 2010, 84(22):11614-11623. doi: 10.1128/JVI.01053-10.
doi: 10.1128/JVI.01053-10
|
[17] |
Hacke K, Rincon-Orozco B, Buchwalter G, et al. Regulation of MCP-1 chemokine transcription by p53[J]. Mol Cancer, 2010, 9:82. doi: 10.1186/1476-4598-9-82.
doi: 10.1186/1476-4598-9-82
|
[18] |
McClellan JL, Davis JM, Steiner JL, et al. Linking tumor-associated macrophages, inflammation, and intestinal tumorigenesis: role of MCP-1[J]. Am J Physiol Gastrointest Liver Physiol, 2012, 303(10):G1087-G1095. doi: 10.1152/ajpgi.00252.2012.
doi: 10.1152/ajpgi.00252.2012
|
[19] |
周超. 肿瘤相关巨噬细胞(TAM)及Tim-3在宫颈癌中的作用及机制研究[D]. 济南:山东大学, 2018.
|
[20] |
Ding H, Cai J, Mao M, et al. Tumor-associated macrophages induce lymphangiogenesis in cervical cancer via interaction with tumor cells[J]. APMIS, 2014, 122(11):1059-1069. doi: 10.1111/apm.12257.
doi: 10.1111/apm.12257
pmid: 24698523
|
[21] |
Hong IS. Stimulatory versus suppressive effects of GM-CSF on tumor progression in multiple cancer types[J]. Exp Mol Med, 2016, 48(7):e242. doi: 10.1038/emm.2016.64.
doi: 10.1038/emm.2016.64
|
[22] |
Lukic A, Larssen P, Fauland A, et al. GM-CSF- and M-CSF-primed macrophages present similar resolving but distinct inflammatory lipid mediator signatures[J]. FASEB J, 2017, 31(10):4370-4381. doi: 10.1096/fj.201700319R.
doi: 10.1096/fj.201700319R
pmid: 28637652
|
[23] |
Liu WH, Liu JJ, Wu J, et al. Retraction: Novel Mechanism of Inhibition of Dendritic Cells Maturation by Mesenchymal Stem Cells via Interleukin-10 and the JAK1/STAT3 Signaling Pathway[J]. PLoS One, 2018, 13(3):e0194455. doi: 10.1371/journal.pone.0194455.
doi: 10.1371/journal.pone.0194455
|
[24] |
Vopenkova K, Mollova K, Buresova I, et al. Complex evaluation of human monocyte-derived dendritic cells for cancer immunotherapy[J]. J Cell Mol Med, 2012, 16(11):2827-2837. doi: 10.1111/j.1582-4934.2012.01614.x.
doi: 10.1111/j.1582-4934.2012.01614.x
pmid: 22882679
|
[25] |
Long J, Hu Z, Xue H, et al. Vascular endothelial growth factor (VEGF) impairs the motility and immune function of human mature dendritic cells through the VEGF receptor 2-RhoA-cofilin1 pathway[J]. Cancer Sci, 2019, 110(8):2357-2367. doi: 10.1111/cas.14091.
doi: 10.1111/cas.14091
|
[26] |
侯萍, 陈龙, 刘艳生. 宫颈癌患者肿瘤浸润性树突状细胞表达水平及其临床意义[J]. 广西医科大学学报, 2017, 34(12):1762-1765. doi: 10.16190/j.cnki.45-1211/r.2017.12.023.
doi: 10.16190/j.cnki.45-1211/r.2017.12.023
|
[27] |
余杨, 邹晶晶. 高危型人乳头状瘤病毒和Th细胞因子与宫颈病变的关系及意义[J]. 中国妇幼卫生杂志, 2016, 7(2):51-54. doi: 10.19757/j.cnki.issn1674-7763.2016.02.014.
doi: 10.19757/j.cnki.issn1674-7763.2016.02.014
|
[28] |
齐涵沁, 朱红芬, 张耀辉. Th1、Th2、Th17、Treg细胞在宫颈癌患者外周血中的变化及意义[J]. 中国妇幼保健, 2017, 32(3):595-597. doi: 10.7620/zgfybj.j.issn.1001-4411.2017.03.61.
doi: 10.7620/zgfybj.j.issn.1001-4411.2017.03.61
|
[29] |
周萍, 冉晓敏. 人乳头瘤病毒感染宫颈病变患者外周血辅助性T17细胞、T细胞和炎症因子的变化及临床意义[J]. 中国妇幼保健, 2019, 34(6):1242-1245. doi: 10.7620/zgfybj.j.issn.1001-4411.2019.06.11.
doi: 10.7620/zgfybj.j.issn.1001-4411.2019.06.11
|
[30] |
Lin W, Zhang HL, Niu ZY, et al. The disease stage-associated imbalance of Th1/Th2 and Th17/Treg in uterine cervical cancer patients and their recovery with the reduction of tumor burden[J]. BMC Womens Health, 2020, 20(1):126. doi: 10.1186/s12905-020-00972-0.
doi: 10.1186/s12905-020-00972-0
|
[31] |
玄秀云, 张月, 雷波, 等. Th22细胞通过释放IL-22活化宫颈癌细胞AKT通路促进其增殖[J]. 免疫学杂志, 2017, 33(10):856-860,866. doi: 10.13431/j.cnki.immunol.j.20170150.
doi: 10.13431/j.cnki.immunol.j.20170150
|
[32] |
田馨莉, 矫俊, 张腾, 等. Th22细胞联合Th17细胞在宫颈癌外周血中的表达及意义[J]. 山东大学学报(医学版), 2015, 53(7):43-47. doi: 10.6040/j.issn.1671-7554.0.2014.964.
doi: 10.6040/j.issn.1671-7554.0.2014.964
|
[33] |
胡云双, 周旺展, 张颖, 等. Th22和Th17细胞在宫颈癌患者外周血中的表达[J]. 温州医科大学学报, 2019, 49(3):210-213. doi: 10.3969/j.issn.2095-9400.2019.03.011.
doi: 10.3969/j.issn.2095-9400.2019.03.011
|
[34] |
王丹红, 张斌, 高海燕, 等. DC诱导CTL治疗HPV感染宫颈癌患者的疗效观察[J]. 中国肿瘤生物治疗杂志, 2014, 21(5):570-573. doi: 10.3872/j.issn.1007-385X.2014.05.016.
doi: 10.3872/j.issn.1007-385X.2014.05.016
|
[35] |
Campo MS, Graham SV, Cortese MS, et al. HPV-16 E5 down-regulates expression of surface HLA class I and reduces recognition by CD8 T cells[J]. Virology, 2010, 407(1):137-142. doi: 10.1016/j.virol.2010.07.044.
doi: 10.1016/j.virol.2010.07.044
pmid: 20813390
|
[36] |
Mehta AM, Jordanova ES, Kenter GG, et al. Association of antigen processing machinery and HLA class I defects with clinicopathological outcome in cervical carcinoma[J]. Cancer Immunol Immunother, 2008, 57(2):197-206. doi: 10.1007/s00262-007-0362-8.
doi: 10.1007/s00262-007-0362-8
|