• 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

供体MHCⅢ类基因在NOD小鼠移植胰岛破坏中的作用

Role of donor MHC class III genes in the destruction of transplanted islets in NOD mice.

作者信息

Jevnikar Anthony M, Prange Sean, Zucker Peter, Singh Bhagirath

机构信息

Department of Microbiology & Immunology, John P. Robarts Research Institute, University of Western Ontario, London, Ontario N6A 5A5, Canada.

出版信息

Ann N Y Acad Sci. 2002 Apr;958:175-8. doi: 10.1111/j.1749-6632.2002.tb02964.x.

DOI:10.1111/j.1749-6632.2002.tb02964.x
PMID:12021101
Abstract

MHC class III genes are important in immune regulation and inflammation, and the gene products of this region are well conserved between species. Their role in diabetes is, however, unknown. We used islets from NOD mice that lacked expression of both MHC class I and class II molecules to test the effect of class III differences on the injury of transplanted NOD islets. Loss of islet MHC class I was highly protective, while deletion of MHC class II had no benefit on islet survival. However the combined absence of both MHC class I and class II expression by NOD islets resulted in a delayed form of injury, when islets were transplanted to NOD mice. As neither MHC class I or II molecules were expressed by donor islet tissue, these results suggest a previously unrecognized and important contribution of MHC class III differences on islet injury following transplantation.

摘要

MHC III类基因在免疫调节和炎症中起重要作用,该区域的基因产物在物种间高度保守。然而,它们在糖尿病中的作用尚不清楚。我们使用缺乏MHC I类和II类分子表达的NOD小鼠胰岛来测试III类差异对移植的NOD胰岛损伤的影响。胰岛MHC I类的缺失具有高度保护作用,而MHC II类的缺失对胰岛存活没有益处。然而,当将胰岛移植到NOD小鼠体内时,NOD胰岛同时缺失MHC I类和II类表达会导致一种延迟性损伤形式。由于供体胰岛组织既不表达MHC I类分子也不表达II类分子,这些结果表明MHC III类差异对移植后胰岛损伤有先前未被认识到的重要贡献。

相似文献

1
Role of donor MHC class III genes in the destruction of transplanted islets in NOD mice.供体MHCⅢ类基因在NOD小鼠移植胰岛破坏中的作用
Ann N Y Acad Sci. 2002 Apr;958:175-8. doi: 10.1111/j.1749-6632.2002.tb02964.x.
2
The role of autoimmunity in islet allograft destruction: major histocompatibility complex class II matching is necessary for autoimmune destruction of allogeneic islet transplants after T-cell costimulatory blockade.自身免疫在胰岛同种异体移植破坏中的作用:在T细胞共刺激阻断后,主要组织相容性复合体II类匹配对于同种异体胰岛移植的自身免疫破坏是必要的。
Diabetes. 2002 Nov;51(11):3202-10. doi: 10.2337/diabetes.51.11.3202.
3
Transplanted MHC class I-deficient nonobese diabetic mouse islets are protected from autoimmune injury in diabetic nonobese recipients.移植的MHC I类缺陷型非肥胖糖尿病小鼠胰岛在糖尿病非肥胖受体中免受自身免疫损伤。
Transplantation. 2001 Apr 15;71(7):982-5. doi: 10.1097/00007890-200104150-00025.
4
"Indirect" acute islet allograft destruction in nonobese diabetic mice is independent of donor major histocompatibility complex and requires host B lymphocytes.非肥胖糖尿病小鼠中“间接”急性胰岛同种异体移植破坏与供体主要组织相容性复合体无关,且需要宿主B淋巴细胞。
Transplant Proc. 2008 Mar;40(2):462-3. doi: 10.1016/j.transproceed.2008.01.054.
5
Recurrent autoimmunity accelerates destruction of minor and major histoincompatible islet grafts in nonobese diabetic (NOD) mice.复发性自身免疫加速非肥胖糖尿病(NOD)小鼠体内次要和主要组织相容性不相容胰岛移植的破坏。
Am J Transplant. 2001 Jul;1(2):138-45.
6
MHC-mismatched islet allografts are vulnerable to autoimmune recognition in vivo.主要组织相容性复合体(MHC)不匹配的胰岛同种异体移植物在体内易受自身免疫识别的影响。
J Immunol. 2005 Aug 15;175(4):2309-16. doi: 10.4049/jimmunol.175.4.2309.
7
Characterization of the role of major histocompatibility complex in type 1 diabetes recurrence after islet transplantation.主要组织相容性复合体在胰岛移植后1型糖尿病复发中作用的特征分析
Transplantation. 2004 Aug 27;78(4):509-15. doi: 10.1097/01.tp.0000128907.83111.c6.
8
Synergy of class I and class II MHC deficiency (C1D and C2D) islets and early short-term suppression in achieving long-term islet graft survival and tolerance induction.I类和II类主要组织相容性复合体缺陷(C1D和C2D)胰岛的协同作用以及早期短期抑制在实现长期胰岛移植存活和诱导耐受性方面的作用。
Transplant Proc. 1999 Feb-Mar;31(1-2):635-6. doi: 10.1016/s0041-1345(98)01591-7.
9
MHC antigen induction by interferon gamma on cultured mouse pancreatic beta cells and macrophages. Genetic analysis of strain differences and discovery of an "occult" class I-like antigen in NOD/Lt mice.干扰素γ对培养的小鼠胰腺β细胞和巨噬细胞的MHC抗原诱导作用。品系差异的遗传分析以及在NOD/Lt小鼠中发现一种“隐匿”的I类样抗原。
J Exp Med. 1989 Oct 1;170(4):1243-62. doi: 10.1084/jem.170.4.1243.
10
Major histocompatibility complex class I-restricted infiltration and destruction of pancreatic islets by NOD mouse-derived beta-cell cytotoxic CD8+ T-cell clones in vivo.在体内,NOD小鼠来源的β细胞细胞毒性CD8 + T细胞克隆对主要组织相容性复合体I类限制的胰岛浸润和破坏。
Diabetes. 1996 Aug;45(8):1121-31. doi: 10.2337/diab.45.8.1121.