• 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

相似文献

1
Borrelia burgdorferi-specific T lymphocytes induce severe destructive Lyme arthritis.伯氏疏螺旋体特异性T淋巴细胞可引发严重的破坏性莱姆关节炎。
Infect Immun. 1995 Apr;63(4):1400-8. doi: 10.1128/iai.63.4.1400-1408.1995.
2
Involvement of CD4+ T lymphocytes in induction of severe destructive Lyme arthritis in inbred LSH hamsters.CD4 + T淋巴细胞在近交系LSH仓鼠严重破坏性莱姆关节炎诱导中的作用。
Infect Immun. 1995 Dec;63(12):4818-25. doi: 10.1128/iai.63.12.4818-4825.1995.
3
Development of destructive arthritis in vaccinated hamsters challenged with Borrelia burgdorferi.接种伯氏疏螺旋体后,接种疫苗的仓鼠出现破坏性关节炎。
Infect Immun. 1994 Jul;62(7):2825-33. doi: 10.1128/iai.62.7.2825-2833.1994.
4
Macrophages exposed to Borrelia burgdorferi induce Lyme arthritis in hamsters.暴露于伯氏疏螺旋体的巨噬细胞会在仓鼠身上引发莱姆关节炎。
Infect Immun. 1996 Jul;64(7):2540-7. doi: 10.1128/iai.64.7.2540-2547.1996.
5
Occurrence of severe destructive lyme arthritis in hamsters vaccinated with outer surface protein A and challenged with Borrelia burgdorferi.用外表面蛋白A疫苗接种并感染伯氏疏螺旋体的仓鼠中出现严重破坏性莱姆关节炎。
Infect Immun. 2000 Feb;68(2):658-63. doi: 10.1128/IAI.68.2.658-663.2000.
6
Macrophages and enriched populations of T lymphocytes interact synergistically for the induction of severe, destructive Lyme arthritis.巨噬细胞与富集的T淋巴细胞群体协同相互作用,以诱导严重的、破坏性的莱姆关节炎。
Infect Immun. 1997 Jul;65(7):2829-36. doi: 10.1128/iai.65.7.2829-2836.1997.
7
Macrophages interact with enriched populations of distinct T lymphocyte subsets for the induction of severe destructive Lyme arthritis.巨噬细胞与不同T淋巴细胞亚群的富集群体相互作用,以诱导严重的破坏性莱姆关节炎。
J Leukoc Biol. 1999 Feb;65(2):162-70. doi: 10.1002/jlb.65.2.162.
8
Isolation of moderately infectious Borrelia burgdorferi sensu stricto from attenuated cultures by using complement-mediated, antibody-dependent lysis selection technique in a mammalian tissue co-culture system.在哺乳动物组织共培养系统中,通过使用补体介导的抗体依赖性裂解选择技术,从减毒培养物中分离出中度传染性的狭义伯氏疏螺旋体。
Microbes Infect. 2003 Aug;5(10):869-78. doi: 10.1016/s1286-4579(03)00178-3.
9
Passive immunization prevents induction of Lyme arthritis in LSH hamsters.被动免疫可预防LSH仓鼠发生莱姆关节炎。
Infect Immun. 1990 Jan;58(1):144-8. doi: 10.1128/iai.58.1.144-148.1990.
10
Association of CD4+ CD25+ T cells with prevention of severe destructive arthritis in Borrelia burgdorferi-vaccinated and challenged gamma interferon-deficient mice treated with anti-interleukin-17 antibody.在接种伯氏疏螺旋体疫苗并受到攻击的γ干扰素缺陷小鼠中,用抗白细胞介素-17抗体治疗后,CD4 + CD25 + T细胞与预防严重破坏性关节炎的关联。
Clin Diagn Lab Immunol. 2004 Nov;11(6):1075-84. doi: 10.1128/CDLI.11.6.1075-1084.2004.

引用本文的文献

1
Immune Response to : Lessons from Lyme Disease Spirochetes.对莱姆病螺旋体的免疫反应:教训。
Curr Issues Mol Biol. 2021;42:145-190. doi: 10.21775/cimb.042.145. Epub 2020 Dec 8.
2
Regulatory T Cells Contribute to Resistance against Lyme Arthritis.调节性 T 细胞有助于抵抗莱姆关节炎。
Infect Immun. 2020 Oct 19;88(11). doi: 10.1128/IAI.00160-20.
3
CD4+ T cells promote antibody production but not sustained affinity maturation during Borrelia burgdorferi infection.在伯氏疏螺旋体感染期间,CD4 + T细胞促进抗体产生,但不促进持续的亲和力成熟。
Infect Immun. 2015 Jan;83(1):48-56. doi: 10.1128/IAI.02471-14. Epub 2014 Oct 13.
4
An Enhanced ELISPOT Assay for Sensitive Detection of Antigen-Specific T Cell Responses to Borrelia burgdorferi.一种增强型 ELISPOT 检测法,用于灵敏检测针对伯氏疏螺旋体的抗原特异性 T 细胞反应。
Cells. 2013 Sep 13;2(3):607-20. doi: 10.3390/cells2030607.
5
Hamster and murine models of severe destructive Lyme arthritis.严重破坏性莱姆关节炎的仓鼠和小鼠模型。
Clin Dev Immunol. 2012;2012:504215. doi: 10.1155/2012/504215. Epub 2012 Feb 22.
6
Interleukin-35 enhances Lyme arthritis in Borrelia-vaccinated and -infected mice.白细胞介素-35增强接种伯氏疏螺旋体疫苗和感染伯氏疏螺旋体小鼠的莱姆关节炎。
Clin Vaccine Immunol. 2011 Jul;18(7):1125-32. doi: 10.1128/CVI.00052-11. Epub 2011 May 25.
7
Activation of gamma delta T cells by Borrelia burgdorferi is indirect via a TLR- and caspase-dependent pathway.伯氏疏螺旋体对γδ T细胞的激活是通过一条依赖Toll样受体(TLR)和半胱天冬酶的间接途径实现的。
J Immunol. 2008 Aug 15;181(4):2392-8. doi: 10.4049/jimmunol.181.4.2392.
8
Interleukin-23 is required for development of arthritis in mice vaccinated and challenged with Borrelia species.用疏螺旋体属疫苗接种并激发的小鼠发生关节炎需要白细胞介素-23。
Clin Vaccine Immunol. 2008 Aug;15(8):1199-207. doi: 10.1128/CVI.00129-08. Epub 2008 Jun 25.
9
Association of CD4+ CD25+ T cells with prevention of severe destructive arthritis in Borrelia burgdorferi-vaccinated and challenged gamma interferon-deficient mice treated with anti-interleukin-17 antibody.在接种伯氏疏螺旋体疫苗并受到攻击的γ干扰素缺陷小鼠中,用抗白细胞介素-17抗体治疗后,CD4 + CD25 + T细胞与预防严重破坏性关节炎的关联。
Clin Diagn Lab Immunol. 2004 Nov;11(6):1075-84. doi: 10.1128/CDLI.11.6.1075-1084.2004.
10
Inhibition of interleukin-17 prevents the development of arthritis in vaccinated mice challenged with Borrelia burgdorferi.抑制白细胞介素-17可预防接种疫苗的小鼠在受到伯氏疏螺旋体攻击后关节炎的发展。
Infect Immun. 2003 Jun;71(6):3437-42. doi: 10.1128/IAI.71.6.3437-3442.2003.

本文引用的文献

1
Induction of interleukin-1 release by high- and low-passage isolates of Borrelia burgdorferi.伯氏疏螺旋体高传代和低传代分离株诱导白细胞介素-1释放
J Infect Dis. 1993 May;167(5):1086-92. doi: 10.1093/infdis/167.5.1086.
2
Long-term study of cell-mediated responses to Borrelia burgdorferi in the laboratory mouse.实验室小鼠对伯氏疏螺旋体细胞介导反应的长期研究。
Infect Immun. 1993 May;61(5):1814-22. doi: 10.1128/iai.61.5.1814-1822.1993.
3
Comparative analysis of using MTT and XTT in colorimetric assays for quantitating bovine neutrophil bactericidal activity.MTT和XTT在比色法中用于定量牛中性粒细胞杀菌活性的比较分析。
J Immunol Methods. 1993 Jan 4;157(1-2):225-31. doi: 10.1016/0022-1759(93)90091-k.
4
Seroprotective groups among isolates of Borrelia burgdorferi.伯氏疏螺旋体分离株中的血清保护组。
Infect Immun. 1993 Oct;61(10):4367-74. doi: 10.1128/iai.61.10.4367-4374.1993.
5
Seroprotective groups of Lyme borreliosis spirochetes from North America and Europe.来自北美和欧洲的莱姆病螺旋体的血清保护组。
J Infect Dis. 1994 Jul;170(1):115-21. doi: 10.1093/infdis/170.1.115.
6
Development of destructive arthritis in vaccinated hamsters challenged with Borrelia burgdorferi.接种伯氏疏螺旋体后,接种疫苗的仓鼠出现破坏性关节炎。
Infect Immun. 1994 Jul;62(7):2825-33. doi: 10.1128/iai.62.7.2825-2833.1994.
7
The T helper cell response in Lyme arthritis: differential recognition of Borrelia burgdorferi outer surface protein A in patients with treatment-resistant or treatment-responsive Lyme arthritis.莱姆关节炎中的辅助性T细胞反应:治疗抵抗性或治疗反应性莱姆关节炎患者对伯氏疏螺旋体外膜蛋白A的差异识别
J Exp Med. 1994 Dec 1;180(6):2069-78. doi: 10.1084/jem.180.6.2069.
8
Preferential usage of T cell antigen receptor V region gene segment V beta 5.1 by Borrelia burgdorferi antigen-reactive T cell clones isolated from a patient with Lyme disease.从一名莱姆病患者分离出的伯氏疏螺旋体抗原反应性T细胞克隆对T细胞抗原受体V区基因片段Vβ5.1的优先使用。
J Immunol. 1993 May 1;150(9):4125-35.
9
Hybridoma cell lines secreting monoclonal antibodies to mouse H-2 and Ia antigens.分泌针对小鼠H-2和Ia抗原的单克隆抗体的杂交瘤细胞系。
J Immunol. 1980 Feb;124(2):533-40.
10
Effect of antithymocyte serum on collagen arthritis in rats: evidence that T cells are involved in its pathogenesis.
Cell Immunol. 1984 Jul;86(2):421-8. doi: 10.1016/0008-8749(84)90397-6.

伯氏疏螺旋体特异性T淋巴细胞可引发严重的破坏性莱姆关节炎。

Borrelia burgdorferi-specific T lymphocytes induce severe destructive Lyme arthritis.

作者信息

Lim L C, England D M, DuChateau B K, Glowacki N J, Schell R F

机构信息

Wisconsin State Laboratory of Hygiene, University of Wisconsin, Madison 53706.

出版信息

Infect Immun. 1995 Apr;63(4):1400-8. doi: 10.1128/iai.63.4.1400-1408.1995.

DOI:10.1128/iai.63.4.1400-1408.1995
PMID:7890402
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC173166/
Abstract

This is the first documentation that Borrelia burgdorferi-specific T lymphocytes are involved in the pathogenesis of Lyme arthritis. We present direct evidence that T lymphocytes obtained from inbred LSH hamsters vaccinated with a whole-cell preparation of Formalin-inactivated B. burgdorferi sensu stricto isolate C-1-11 in adjuvant conferred on naive recipient hamsters the ability to develop severe destructive arthritis when challenged with B. burgdorferi sensu stricto isolates C-1-11 and 297. By contrast, recipients infused with normal T lymphocytes and challenged with B. burgdorferi sensu stricto isolates C-1-11 and 297 failed to develop severe destructive arthritis. The T lymphocytes transferred were obtained from the lymph nodes of vaccinated and nonvaccinated hamsters by depleting B lymphocytes by using monoclonal antibody 14-4-4s (< 1% B lymphocytes by flow cytometric analysis). The enriched T lymphocytes showed enhanced proliferation to stimulation with concanavalin A and failed to respond to lipopolysaccharide. Moreover, only the enriched T lymphocytes from vaccinated hamsters proliferated on exposure to a whole-cell preparation of B. burgdorferi sensu stricto isolate C-1-11 in the presence of mitomycin-treated syngeneic antigen-presenting cells. These results demonstrate that B. burgdorferi-specific T lymphocytes primed by vaccination with a whole-cell preparation of inactivated B. burgdorferi sensu stricto isolate C-1-11 in adjuvant are involved in the development of severe destructive arthritis. Additional experiments are needed to define the precise mechanism(s) responsible for the development of Lyme arthritis.

摘要

这是关于伯氏疏螺旋体特异性T淋巴细胞参与莱姆关节炎发病机制的首次文献记载。我们提供了直接证据,即从用福尔马林灭活的伯氏疏螺旋体狭义种C-1-11全细胞制剂加佐剂免疫的近交系LSH仓鼠中获得的T淋巴细胞,在给未免疫的受体仓鼠接种伯氏疏螺旋体狭义种C-1-11和297后,赋予了它们发生严重破坏性关节炎的能力。相比之下,输注正常T淋巴细胞并接种伯氏疏螺旋体狭义种C-1-11和297的受体仓鼠未发生严重破坏性关节炎。转移的T淋巴细胞是通过使用单克隆抗体14-4-4s清除B淋巴细胞(通过流式细胞术分析B淋巴细胞<1%),从免疫和未免疫仓鼠的淋巴结中获得的。富集的T淋巴细胞对刀豆球蛋白A刺激的增殖增强,对脂多糖无反应。此外,只有来自免疫仓鼠的富集T淋巴细胞在丝裂霉素处理的同基因抗原呈递细胞存在的情况下,接触伯氏疏螺旋体狭义种C-1-11全细胞制剂时才会增殖。这些结果表明,用福尔马林灭活的伯氏疏螺旋体狭义种C-1-11全细胞制剂加佐剂免疫引发的伯氏疏螺旋体特异性T淋巴细胞参与了严重破坏性关节炎的发展。需要进一步的实验来确定导致莱姆关节炎发展的确切机制。