• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

B16黑色素瘤表达B7共刺激分子会引发自然杀伤细胞依赖性的局部抗肿瘤反应,但仅诱导针对表达B7肿瘤的T细胞依赖性全身免疫。

Expression of B7 co-stimulatory molecules by B16 melanoma results in a natural killer cell-dependent local anti-tumour response, but induces T-cell-dependent systemic immunity only against B7-expressing tumours.

作者信息

Chong H, Hutchinson G, Hart I R, Vile R G

机构信息

Department of Histopathology, United Medical and Dental Schools of Guy's and St. Thomas's Hospitals, London, UK.

出版信息

Br J Cancer. 1998 Oct;78(8):1043-50. doi: 10.1038/bjc.1998.625.

DOI:10.1038/bjc.1998.625
PMID:9792148
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2063155/
Abstract

In an attempt to enhance the anti-tumour immune response, the co-stimulatory molecules B7-1 or B7-2 were expressed on the surface of B16 melanoma cells. B7-expressing tumours grew more slowly in both syngeneic immunocompetent mice and athymic T cell-immunodeficient nude mice. The delay in growth of B7-expressing tumours was dependent on natural killer (NK) cells, as reductions in tumour growth rates were minimized in mice depleted of NK cells. Systemic immunity to B16 melanoma was examined by vaccination with irradiated tumour cells. Inoculation with irradiated B16 B7-1 cells failed to protect against a subsequent challenge with live parental B16 cells, but conferred partial protection against challenge with live B16 B7-1 cells. In contrast to the local anti-tumour reaction, this protective response was dependent on T cells. The results presented here reveal some of the mechanisms involved in the in vivo response to a poorly immunogenic tumour modified to express co-stimulatory molecules.

摘要

为增强抗肿瘤免疫反应,共刺激分子B7-1或B7-2在B16黑色素瘤细胞表面表达。在同基因免疫活性小鼠和无胸腺T细胞免疫缺陷裸鼠中,表达B7的肿瘤生长均较为缓慢。表达B7的肿瘤生长延迟依赖于自然杀伤(NK)细胞,因为在NK细胞耗竭的小鼠中,肿瘤生长速率的降低最小化。通过用辐照肿瘤细胞进行疫苗接种来检测对B16黑色素瘤的全身免疫。接种辐照的B16 B7-1细胞未能预防随后活的亲代B16细胞的攻击,但对活的B16 B7-1细胞的攻击提供了部分保护。与局部抗肿瘤反应相反,这种保护性反应依赖于T细胞。此处呈现的结果揭示了体内对经修饰以表达共刺激分子的低免疫原性肿瘤的反应所涉及的一些机制。

相似文献

1
Expression of B7 co-stimulatory molecules by B16 melanoma results in a natural killer cell-dependent local anti-tumour response, but induces T-cell-dependent systemic immunity only against B7-expressing tumours.B16黑色素瘤表达B7共刺激分子会引发自然杀伤细胞依赖性的局部抗肿瘤反应,但仅诱导针对表达B7肿瘤的T细胞依赖性全身免疫。
Br J Cancer. 1998 Oct;78(8):1043-50. doi: 10.1038/bjc.1998.625.
2
Interleukin-18 and the costimulatory molecule B7-1 have a synergistic anti-tumor effect on murine melanoma; implication of combined immunotherapy for poorly immunogenic malignancy.白细胞介素-18与共刺激分子B7-1对小鼠黑色素瘤具有协同抗肿瘤作用;对免疫原性低下的恶性肿瘤进行联合免疫治疗的意义。
J Invest Dermatol. 2000 May;114(5):928-34. doi: 10.1038/sj.jid.5600685.
3
Enhancing CTL responses to melanoma cell vaccines in vivo: synergistic increases obtained using IFNgamma primed and IFNbeta treated B7-1+ B16-F10 melanoma cells.增强体内针对黑色素瘤细胞疫苗的细胞毒性T淋巴细胞反应:使用经γ干扰素预刺激和β干扰素处理的B7-1+B16-F10黑色素瘤细胞获得协同增强效果。
Immunol Cell Biol. 2003 Dec;81(6):459-71. doi: 10.1046/j.0818-9641.2003.01189.x.
4
Expression of co-stimulatory molecules by tumor cells decreases tumorigenicity but may also reduce systemic antitumor immunity.肿瘤细胞共刺激分子的表达可降低致瘤性,但也可能降低全身抗肿瘤免疫力。
Hum Gene Ther. 1996 Sep 10;7(14):1771-9. doi: 10.1089/hum.1996.7.14-1771.
5
Enhancement of effector CD8+ T-cell function by tumour-associated B7-H3 and modulation of its counter-receptor triggering receptor expressed on myeloid cell-like transcript 2 at tumour sites.肿瘤相关 B7-H3 通过调节肿瘤部位髓样细胞样转录物 2 表达的触发受体增强效应 CD8+ T 细胞功能。
Immunology. 2010 Jul;130(3):363-73. doi: 10.1111/j.1365-2567.2009.03236.x. Epub 2010 Feb 5.
6
Gene transfer of the Co-stimulatory molecules B7-1 and B7-2 enhances the immunogenicity of human renal cell carcinoma to a different extent.共刺激分子B7-1和B7-2的基因转移在不同程度上增强了人肾细胞癌的免疫原性。
Scand J Immunol. 1999 Sep;50(3):242-9. doi: 10.1046/j.1365-3083.1999.00588.x.
7
Expression of MHC Class II and B7-1 and B7-2 costimulatory molecules accompanies tumor rejection and reduces the metastatic potential of tumor cells.MHC II类分子以及共刺激分子B7-1和B7-2的表达伴随着肿瘤排斥反应,并降低肿瘤细胞的转移潜能。
Tissue Antigens. 1996 May;47(5):414-21. doi: 10.1111/j.1399-0039.1996.tb02577.x.
8
T cell activation by antigens on human melanoma cells--co-stimulation by B7-1 is neither sufficient nor necessary to stimulate IL-2 secretion by melanoma-specific T cell clones in vitro.人黑色素瘤细胞上的抗原激活T细胞——在体外,B7 - 1的共刺激对于刺激黑色素瘤特异性T细胞克隆分泌白细胞介素-2既不充分也不必要。
Int Immunol. 1995 Oct;7(10):1535-43. doi: 10.1093/intimm/7.10.1535.
9
Interaction between B.7 and CD28 costimulatory molecules is essential for the activation of effector function mediating spontaneous tumour regression.B.7与CD28共刺激分子之间的相互作用对于介导自发性肿瘤消退的效应器功能的激活至关重要。
Scand J Immunol. 1999 Jun;49(6):633-40. doi: 10.1046/j.1365-3083.1999.00550.x.
10
IL-12-activated NK cells recognize B7 costimulatory molecules on tumor cells and autologous dendritic cells.
Adv Exp Med Biol. 1998;451:203-10. doi: 10.1007/978-1-4615-5357-1_32.

引用本文的文献

1
Differences in Co-Expression of T Cell Co-Inhibitory and Co-Stimulatory Molecules with PD-1 Across Different Human Cancers.不同人类癌症中T细胞共抑制和共刺激分子与PD-1共表达的差异。
J Oncol Res Ther. 2024;9(2). doi: 10.29011/2574-710x.10224. Epub 2024 Jun 10.
2
EGR3 Inhibits Tumor Progression by Inducing Schwann Cell-Like Differentiation.EGR3 通过诱导施万细胞样分化抑制肿瘤进展。
Adv Sci (Weinh). 2024 Sep;11(34):e2400066. doi: 10.1002/advs.202400066. Epub 2024 Jul 7.
3
cis-B7:CD28 interactions at invaginated synaptic membranes provide CD28 co-stimulation and promote CD8 T cell function and anti-tumor immunity.内陷突触膜上的 cis-B7:CD28 相互作用提供 CD28 共刺激作用,促进 CD8 T 细胞功能和抗肿瘤免疫。
Immunity. 2023 Jun 13;56(6):1187-1203.e12. doi: 10.1016/j.immuni.2023.04.005. Epub 2023 May 8.
4
Engineered Cell-Membrane-Coated Nanoparticles Directly Present Tumor Antigens to Promote Anticancer Immunity.工程化细胞膜包覆纳米颗粒直接呈递肿瘤抗原以促进抗癌免疫。
Adv Mater. 2020 Jul;32(30):e2001808. doi: 10.1002/adma.202001808. Epub 2020 Jun 15.
5
Induction of an antitumour adaptive immune response elicited by tumour cells expressing de novo B7-1 mainly depends on the anatomical site of their delivery: the dose applied regulates the expansion of the response.由从头表达B7-1的肿瘤细胞引发的抗肿瘤适应性免疫反应的诱导主要取决于其递送的解剖部位:所应用的剂量调节反应的扩展。
Immunology. 2003 Dec;110(4):474-81. doi: 10.1111/j.1365-2567.2003.01760.x.
6
B7H costimulates clonal expansion of, and cognate destruction of tumor cells by, CD8(+) T lymphocytes in vivo.B7H在体内共刺激CD8(+) T淋巴细胞对肿瘤细胞进行克隆扩增并对其进行同源性杀伤。
J Exp Med. 2001 Nov 5;194(9):1339-48. doi: 10.1084/jem.194.9.1339.
7
The heat-stable antigen determines pathogenicity of self-reactive T cells in experimental autoimmune encephalomyelitis.热稳定抗原决定实验性自身免疫性脑脊髓炎中自身反应性T细胞的致病性。
J Clin Invest. 2000 May;105(9):1227-32. doi: 10.1172/JCI9012.

本文引用的文献

1
Generation of an anti-tumour immune response in a non-immunogenic tumour: HSVtk killing in vivo stimulates a mononuclear cell infiltrate and a Th1-like profile of intratumoural cytokine expression.在非免疫原性肿瘤中产生抗肿瘤免疫反应:体内单纯疱疹病毒胸苷激酶(HSVtk)杀伤作用可刺激单核细胞浸润及肿瘤内细胞因子表达呈现Th1样特征。
Int J Cancer. 1997 Apr 10;71(2):267-74. doi: 10.1002/(sici)1097-0215(19970410)71:2<267::aid-ijc23>3.0.co;2-d.
2
Influence of gene-modified (IL-7, IL-4, and B7) tumor cell vaccines on tumor antigen presentation.基因修饰(白细胞介素-7、白细胞介素-4和B7)肿瘤细胞疫苗对肿瘤抗原呈递的影响。
J Immunol. 1997 Mar 15;158(6):2834-41.
3
Identification of tyrosinase-related protein 2 as a tumor rejection antigen for the B16 melanoma.鉴定酪氨酸酶相关蛋白2为B16黑色素瘤的肿瘤排斥抗原。
J Exp Med. 1997 Feb 3;185(3):453-9. doi: 10.1084/jem.185.3.453.
4
Immunotherapy I: Cyclosine gene transfer strategies.免疫疗法I:环孢素基因转移策略。
Cancer Metastasis Rev. 1996 Sep;15(3):317-28. doi: 10.1007/BF00046345.
5
Immune response to a differentiation antigen induced by altered antigen: a study of tumor rejection and autoimmunity.由改变的抗原诱导的对分化抗原的免疫反应:肿瘤排斥与自身免疫的研究
Proc Natl Acad Sci U S A. 1996 Dec 10;93(25):14809-14. doi: 10.1073/pnas.93.25.14809.
6
Expression of co-stimulatory molecules by tumor cells decreases tumorigenicity but may also reduce systemic antitumor immunity.肿瘤细胞共刺激分子的表达可降低致瘤性,但也可能降低全身抗肿瘤免疫力。
Hum Gene Ther. 1996 Sep 10;7(14):1771-9. doi: 10.1089/hum.1996.7.14-1771.
7
Triggering of natural killer cells by the costimulatory molecule CD80 (B7-1).共刺激分子CD80(B7-1)对自然杀伤细胞的激活
Immunity. 1996 Oct;5(4):311-7. doi: 10.1016/s1074-7613(00)80257-5.
8
Allogeneic lymphocyte responses to B7-1 expressing human cancer cell lines.对表达B7-1的人癌细胞系的同种异体淋巴细胞反应。
J Surg Res. 1996 Jul 15;64(1):42-8. doi: 10.1006/jsre.1996.0304.
9
Does B7-1 expression confer antigen-presenting cell capacity to tumors in vivo?B7-1的表达是否赋予肿瘤在体内呈现抗原的细胞能力?
J Exp Med. 1996 Mar 1;183(3):769-76. doi: 10.1084/jem.183.3.769.
10
Irradiated B7-1 transduced primary acute myelogenous leukemia (AML) cells can be used as therapeutic vaccines in murine AML.经照射的转导B7-1的原发性急性髓性白血病(AML)细胞可作为小鼠AML的治疗性疫苗。
Blood. 1996 Apr 1;87(7):2938-46.