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1型糖尿病与免疫耐受 被引量：2

Type 1 diabetes and immune tolerance
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摘要 1型糖尿病是一种自身免疫性疾病,免疫系统选择性攻击胰腺中的胰岛β细胞,导致β细胞的损害以及胰岛素的绝对缺乏.虽然临床上1型糖尿病的发病是一个突发事件,但根据对1型糖尿病患者发病的跟踪研究发现,在出现高血糖的几年前就可检测到患者体内存在抗胰岛细胞自身抗体,通常在发病的1a前,葡萄糖耐量试验也会发生恶化.因此,通过应用1型糖尿病动物模型,研究明显糖尿病出现前机体的异常变化,有助于深入了解糖尿病发病机制,为预防或治疗1型糖尿病提供科学依据.本文主要以NOD小鼠为例,总结了机体免疫耐受在维持自身稳定、调节免疫平衡中的机制和NOD小鼠免疫耐受的缺陷及其对糖尿病发病的影响.
作者 孙纳新 杨桂文 安利国
机构地区 山东师范大学生命科学学院动物抗性重点实验室
出处 《世界华人消化杂志》 CAS 北大核心 2005年第16期2001-2003,共3页 World Chinese Journal of Digestology
基金 山东省自然科学基金资助课题 No.Z2003D01
关键词 1型糖尿病 免疫耐受 自身免疫性疾病 抗胰岛细胞自身抗体 病发病机制 葡萄糖耐量试验 胰岛Β细胞 糖尿病患者 NOD小鼠
分类号 R587.1 [医药卫生—内分泌] R392.4 [医药卫生—免疫学]
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参考文献26

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同被引文献29

  • 1童金生.CD26／DPPIV结构和功能研究进展[J].国际免疫学杂志,2007,30(1):39-42. 被引量：4
  • 2陈海冰,贾伟平.糖尿病与免疫[J].临床内科杂志,2007,24(3):159-161. 被引量：14
  • 3Ugur Aytac, Nam H. Dang CD26/Dipeptidyl peptidase IV:A regulator of immune function and a potential molecular target for Therapy [ J ]. Current Drug Targets-Immune, Endocrine Metabolic Disorders, 2004,4 : 11 - 18.
  • 4Seiji Kobayashi, Kei Ohnunm, Masahiko Uchiyama. Association of CD26 with CD45RA outside lipid rafts attenuates cord blood T-cell activation [ J ]. Blood ,2004,103:228 - 234.
  • 5Kathleen Aertgeets, Sheng ye, Lihong SHI, et al. N-linked glycosylation of dipeptidyI peptidase g (CD26) :Effects on enzyme activity homodimer formation and adenosine deaminase binding protein [ J ]. Science,2004, 13 : 145 - 154.
  • 6Pacheco R, Martinez-Navio J M, Lejeune M. CD26, adenosine deami- nase, and adenosine receptors mediate costimulatory signalsin the immu- nological synapse [ J ]. PNAS,2005,102:9583 - 9584.
  • 7Kholova I, Hldvikova M, Ryska A, et al. Immunobisto chemical detection of dipeptidyl peptidase IV ( CD 26) in thyroid neoplasia using biotinylated tyramine amplification [ J ]. Neoplasma,2003,50 : 159 - 164.
  • 8Khin EE, Kikkawa F, Ino K, et al. Dipeptidyl peptidase IV expression in endometrial endometriold adenocarcinoma and its inverse correlation with tumor grade[J]. Am J Obstet Gynecol,2003,188(3) :670 -676.
  • 9Kholova I, Ludvikova M, Ryska A. Diagnoistic role of markers DipeptidyI peptidase 4 and thyroid peroxidase in throid tumors[ J]. Anticancer Rds, 2003,23:871 - 875.
  • 10Alard P, Manirarora JN, Parnell SA, et al Deficiency in NOD antigenpr- esenting cell function may be responsible for suboptimal CIM + CD25 + T-cell-mediated refulation and rype 1 diabetes deve; opment in NOD mice [ J]. Diabetes,2006,55:2098 - 2105.

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世界华人消化杂志
2005年 第16期

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