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本文引用的文献

1
IL-10 expression is regulated by HPV E2 protein in cervical cancer cells.白细胞介素-10 的表达受 HPV E2 蛋白在宫颈癌中的调控。
Mol Med Rep. 2011 Mar-Apr;4(2):369-75. doi: 10.3892/mmr.2011.429. Epub 2011 Jan 25.
2
The role of interleukin-12 on modulating myeloid-derived suppressor cells, increasing overall survival and reducing metastasis.白细胞介素-12 在调节髓源性抑制细胞、提高总生存率和减少转移中的作用。
Immunology. 2011 Jun;133(2):221-38. doi: 10.1111/j.1365-2567.2011.03429.x. Epub 2011 Apr 1.
3
Gene therapy with interleukin-10 receptor and interleukin-12 induces a protective interferon-γ-dependent response against B16F10-Nex2 melanoma.白细胞介素-10 受体和白细胞介素-12 的基因治疗诱导针对 B16F10-Nex2 黑色素瘤的保护性干扰素-γ 依赖性反应。
Cancer Gene Ther. 2011 Feb;18(2):110-22. doi: 10.1038/cgt.2010.58. Epub 2010 Oct 1.
4
Antitumor mechanism of recombinant murine interleukin-12 vaccine.重组鼠白细胞介素-12 疫苗的抗肿瘤机制。
Cancer Biother Radiopharm. 2010 Jun;25(3):263-8. doi: 10.1089/cbr.2010.0771.
5
Interleukin-10 production by tumor infiltrating macrophages plays a role in Human Papillomavirus 16 tumor growth.肿瘤浸润巨噬细胞产生的白细胞介素-10 在人乳头瘤病毒 16 肿瘤生长中发挥作用。
BMC Immunol. 2010 Jun 7;11:27. doi: 10.1186/1471-2172-11-27.
6
HPV16 tumor associated macrophages suppress antitumor T cell responses.人乳头瘤病毒16型肿瘤相关巨噬细胞抑制抗肿瘤T细胞反应。
Clin Cancer Res. 2009 Jul 1;15(13):4391-400. doi: 10.1158/1078-0432.CCR-09-0489. Epub 2009 Jun 23.
7
Conditional interleukin-12 gene therapy promotes safe and effective antitumor immunity.条件性白细胞介素-12 基因治疗促进安全有效的抗肿瘤免疫。
Cancer Gene Ther. 2009 Dec;16(12):883-91. doi: 10.1038/cgt.2009.33. Epub 2009 May 15.
8
HPV 16 E2 protein induces apoptosis in human and murine HPV 16 transformed epithelial cells and has antitumoral effects in vivo.人乳头瘤病毒16型E2蛋白可诱导人和鼠类人乳头瘤病毒16型转化上皮细胞发生凋亡,并在体内具有抗肿瘤作用。
Tumour Biol. 2009;30(2):61-72. doi: 10.1159/000214438. Epub 2009 Apr 22.
9
Modulation of apoptosis by early human papillomavirus proteins in cervical cancer.人乳头瘤病毒早期蛋白对宫颈癌细胞凋亡的调控作用
Biochim Biophys Acta. 2010 Jan;1805(1):6-16. doi: 10.1016/j.bbcan.2009.03.005. Epub 2009 Apr 15.
10
CD3zeta expression and T cell proliferation are inhibited by TGF-beta1 and IL-10 in cervical cancer patients.在宫颈癌患者中,转化生长因子-β1(TGF-β1)和白细胞介素-10(IL-10)可抑制CD3ζ表达和T细胞增殖。
J Clin Immunol. 2009 Jul;29(4):532-44. doi: 10.1007/s10875-009-9279-7. Epub 2009 Mar 4.

阻断 HPV 诱导损伤发展的分子机制及潜在靶点。

Molecular Mechanism and Potential Targets for Blocking HPV-Induced Lesion Development.

机构信息

Division of Chronic Infections and Cancer, Research Center for Infectious Diseases, Instituto Nacional de Salud Pública, Avenida Universidad No. 655, Cuernavaca 62100, Morelos, Mexico.

出版信息

J Oncol. 2012;2012:278312. doi: 10.1155/2012/278312. Epub 2011 Dec 19.

DOI:10.1155/2012/278312
PMID:22220169
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3246776/
Abstract

Persistent infection with high-risk HPV is the etiologic agent associated with the development of cervical cancer (CC) development. However, environmental, social, epidemiological, genetic, and host factors may have a joint influence on the risk of disease progression. Cervical lesions caused by HPV infection can be removed naturally by the host immune response and only a small percentage may progress to cancer; thus, the immune response is essential for the control of precursor lesions and CC. We present a review of recent research on the molecular mechanisms that allow HPV-infected cells to evade immune surveillance and potential targets of molecular therapy to inhibit tumor immune escape.

摘要

高危型 HPV 的持续感染是与宫颈癌 (CC) 发展相关的病因。然而,环境、社会、流行病学、遗传和宿主因素可能对疾病进展的风险有共同影响。HPV 感染引起的宫颈病变可以被宿主免疫反应自然清除,只有一小部分可能进展为癌症;因此,免疫反应对于控制癌前病变和 CC 是至关重要的。我们综述了最近关于 HPV 感染细胞逃避免疫监视的分子机制以及抑制肿瘤免疫逃逸的分子治疗潜在靶点的研究。