• 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

在肺内,腺病毒介导的KARAP/DAP12过表达可增强侵袭性曲霉病期间的真菌清除率。

Intrapulmonary, adenovirus-mediated overexpression of KARAP/DAP12 enhances fungal clearance during invasive aspergillosis.

作者信息

Carpenter Kristin J, Buckland Karen F, Xing Zhou, Hogaboam Cory M

机构信息

Department of Pathology, University of Michigan Medical School, Rm. 5216B, Med. Sci. I, 1301 Catherine Road, Ann Arbor, MI 48109-0602, USA.

出版信息

Infect Immun. 2005 Dec;73(12):8402-6. doi: 10.1128/IAI.73.12.8402-8406.2005.

DOI:10.1128/IAI.73.12.8402-8406.2005
PMID:16299339
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1307040/
Abstract

Herein, we report that the intrapulmonary delivery of an adenovirus vector expressing KARAP/DAP12, an adaptor protein expressed in granulocytes and mononuclear cells, enhanced fungal clearance during experimental invasive pulmonary aspergillosis in neutropenic mice.

摘要

在此,我们报告,在中性粒细胞减少的小鼠实验性侵袭性肺曲霉病期间,表达KARAP/DAP12(一种在粒细胞和单核细胞中表达的衔接蛋白)的腺病毒载体经肺内递送可增强真菌清除。

相似文献

1
Intrapulmonary, adenovirus-mediated overexpression of KARAP/DAP12 enhances fungal clearance during invasive aspergillosis.在肺内,腺病毒介导的KARAP/DAP12过表达可增强侵袭性曲霉病期间的真菌清除率。
Infect Immun. 2005 Dec;73(12):8402-6. doi: 10.1128/IAI.73.12.8402-8406.2005.
2
Innate immune activation and CD4+ T cell priming during respiratory fungal infection.呼吸道真菌感染期间的固有免疫激活和CD4+T细胞致敏
Immunity. 2006 Oct;25(4):665-75. doi: 10.1016/j.immuni.2006.08.016. Epub 2006 Oct 5.
3
The bug in MyD88 dependency.
Immunity. 2006 Oct;25(4):527-9. doi: 10.1016/j.immuni.2006.09.004.
4
Role of TNF-alpha in pulmonary host defense in murine invasive aspergillosis.肿瘤坏死因子-α在小鼠侵袭性曲霉病肺部宿主防御中的作用
J Immunol. 1999 Feb 1;162(3):1633-40.
5
Macrophage inflammatory protein-1 alpha is a critical mediator of host defense against invasive pulmonary aspergillosis in neutropenic hosts.巨噬细胞炎性蛋白-1α是中性粒细胞减少宿主抵御侵袭性肺曲霉病的关键介质。
J Immunol. 2000 Jul 15;165(2):962-8. doi: 10.4049/jimmunol.165.2.962.
6
Transient overexpression of gamma interferon promotes Aspergillus clearance in invasive pulmonary aspergillosis.γ干扰素的瞬时过表达促进侵袭性肺曲霉病中曲霉菌的清除。
Clin Exp Immunol. 2005 Nov;142(2):233-41. doi: 10.1111/j.1365-2249.2005.02828.x.
7
Experimental pulmonary aspergillosis in sensitized rabbits.致敏兔的实验性肺曲霉病
Morphol Embryol (Bucur). 1977 Jul-Sep;23(3):207-15.
8
Polymorphisms in toll-like receptor genes and susceptibility to pulmonary aspergillosis.Toll样受体基因多态性与肺曲霉病易感性
J Infect Dis. 2008 Feb 15;197(4):618-21. doi: 10.1086/526500.
9
Role of Toll-like receptors in lung innate defense against invasive aspergillosis. Distinct impact in immunocompetent and immunocompromized hosts.Toll样受体在肺部抗侵袭性曲霉病天然防御中的作用。对免疫功能正常和免疫功能低下宿主的不同影响。
Clin Immunol. 2007 Sep;124(3):238-43. doi: 10.1016/j.clim.2007.05.004. Epub 2007 Jul 2.
10
Protective role of mannan-binding lectin in a murine model of invasive pulmonary aspergillosis.甘露聚糖结合凝集素在侵袭性肺曲霉病小鼠模型中的保护作用。
Clin Exp Immunol. 2007 May;148(2):382-9. doi: 10.1111/j.1365-2249.2007.03351.x. Epub 2007 Mar 5.

引用本文的文献

1
Fatal outcome of pandemic H1N1 2009 influenza virus infection is associated with immunopathology and impaired lung repair, not enhanced viral burden, in pregnant mice.大流行性 H1N1 2009 流感病毒感染的致命结局与免疫病理学和肺修复受损有关,而不是病毒载量增加,在怀孕小鼠中。
J Virol. 2011 Nov;85(21):11208-19. doi: 10.1128/JVI.00654-11. Epub 2011 Aug 24.
2
Triggering receptor expressed on myeloid cells-1 (TREM-1) modulates immune responses to Aspergillus fumigatus during fungal asthma in mice.髓系细胞表达的触发受体 1(TREM-1)调节小鼠真菌性哮喘期间烟曲霉的免疫反应。
Immunol Invest. 2011;40(7-8):692-722. doi: 10.3109/08820139.2011.578270. Epub 2011 May 19.

本文引用的文献

1
Brain and bone damage in KARAP/DAP12 loss-of-function mice correlate with alterations in microglia and osteoclast lineages.KARAP/DAP12功能缺失小鼠的脑和骨损伤与小胶质细胞和破骨细胞谱系的改变相关。
Am J Pathol. 2005 Jan;166(1):275-86. doi: 10.1016/S0002-9440(10)62251-1.
2
Cutting edge: expression patterns of surface and soluble triggering receptor expressed on myeloid cells-1 in human endotoxemia.前沿:人类内毒素血症中髓系细胞表面和可溶性触发受体-1的表达模式
J Immunol. 2004 Dec 15;173(12):7131-4. doi: 10.4049/jimmunol.173.12.7131.
3
Role of CCR4 ligands, CCL17 and CCL22, during Schistosoma mansoni egg-induced pulmonary granuloma formation in mice.CCR4配体CCL17和CCL22在曼氏血吸虫卵诱导的小鼠肺部肉芽肿形成过程中的作用。
Am J Pathol. 2004 Oct;165(4):1211-21. doi: 10.1016/S0002-9440(10)63381-0.
4
Triggering receptor expressed on myeloid cells: role in the diagnosis of lung infections.髓系细胞上表达的触发受体:在肺部感染诊断中的作用
Eur Respir J. 2004 Aug;24(2):247-50. doi: 10.1183/09031936.04.00014204.
5
Expression of TREM-1 mRNA in acute pancreatitis.急性胰腺炎中触发受体表达分子-1(TREM-1)信使核糖核酸(mRNA)的表达
World J Gastroenterol. 2004 Sep 15;10(18):2744-6. doi: 10.3748/wjg.v10.i18.2744.
6
Plasma level of a triggering receptor expressed on myeloid cells-1: its diagnostic accuracy in patients with suspected sepsis.髓系细胞表达的触发受体-1的血浆水平:其在疑似脓毒症患者中的诊断准确性
Ann Intern Med. 2004 Jul 6;141(1):9-15. doi: 10.7326/0003-4819-141-1-200407060-00009.
7
Differential regulation of DAP12 and molecules associated with DAP12 during host responses to mycobacterial infection.宿主对分枝杆菌感染的反应过程中DAP12及与DAP12相关分子的差异调节。
Infect Immun. 2004 May;72(5):2477-83. doi: 10.1128/IAI.72.5.2477-2483.2004.
8
Triggering receptor expressed on myeloid cells-1 in neutrophil inflammatory responses: differential regulation of activation and survival.髓样细胞表达的触发受体-1在中性粒细胞炎症反应中的作用:激活与存活的差异调节
J Immunol. 2004 Apr 15;172(8):4956-63. doi: 10.4049/jimmunol.172.8.4956.
9
Soluble triggering receptor expressed on myeloid cells and the diagnosis of pneumonia.髓系细胞上表达的可溶性触发受体与肺炎的诊断
N Engl J Med. 2004 Jan 29;350(5):451-8. doi: 10.1056/NEJMoa031544.
10
CCL17 and IL-10 as effectors that enable alternatively activated macrophages to inhibit the generation of classically activated macrophages.CCL17和IL-10作为效应因子,可使交替活化的巨噬细胞抑制经典活化巨噬细胞的产生。
J Immunol. 2004 Feb 1;172(3):1407-13. doi: 10.4049/jimmunol.172.3.1407.