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NOD/ShiLtJ
品系货号:001976 | 通用名称:NOD
又名:非肥胖型糖尿病小鼠
摘要
NOD/ShiLtJ 品系(通常称为 NOD 品系)是自身免疫性 1 型糖尿病的多基因模型。NOD 小鼠的糖尿病表现为高血糖症和胰岛炎(胰岛可见白细胞浸润)。雌鼠在约 12 周龄时发生胰腺胰岛素含量显著降低,该现象在雄鼠中发生时间要晚数周。2017 年的一项表型研究发现,90% 的雌鼠和 52% 的雄鼠到 30 周龄时出现糖尿病;雌鼠发病中位时间为 18 周龄。NOD 背景中的免疫表型缺陷包括以下几方面:抗原呈递、T 淋巴细胞库、NK 细胞功能、巨噬细胞细胞因子分泌、伤口愈合和 C5 补体。这些缺陷使 NOD 背景成为免疫缺陷小鼠品系的共同选择。您可以浏览我们的糖尿病发病数据

我们的临床前疗效检测服务可为您提供科学的专业知识以及一系列基于靶标和表型的检测结果(包括体内和终点指标),可用于对糖尿病小鼠模型进行灵活的研究设计和方法开发。欢迎查看我们的全方位服务平台
重要提示:This strain is homozygous for Cdh23ahl, the age related hearing loss 1 mutation, which on this background results in progressive hearing loss that is already severe by three months of age.
品系特点
原始参考文献
Info 当使用该小鼠品系发表文献时,请引用原始文献,并在材料方法中提供该品系的品系货号:JAX stock#001976
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品系详情
NOD/ShiLtJ 小鼠的糖尿病表现为胰岛炎(胰岛可见白细胞浸润)。雌鼠在约 12 周龄时出现胰腺胰岛素含量显著降低,该现象在雄鼠中发生时间要晚数周。糖尿病发病指标为中度糖尿,以及非空腹血糖高于 250 mg/dL。糖尿病小鼠具有低胰岛素血症和高胰高血糖素血症,提示胰岛 β 细胞有选择性功能损伤。NOD/ShiLtJ 小鼠对 IDDM 的易感性是多基因共同影响的结果,同时环境(包括笼养条件、健康状况和饲料)对外显率也有较强影响。NOD/ShiLtJ 雌鼠比雄鼠的应用更广,因为雌鼠的 IDDM 症状发作时间更早,发病率更高(30 周龄时达 90-100%)。NOD/ShiLtJ 雄鼠在 30-40 周龄时的 IDDM 发病率仅 40-60%。不过,雄鼠也有很大用途,包括药物研究、IDDM“加速转运”和一些体外研究。造成 NOD 小鼠对糖尿病易感的主要原因是其特有的 MHC 单体型(H2g7 = Kd、Aad、Abg7、Enull、Db)。NOD 小鼠还具有多种异常免疫表型表现,包括抗原呈递细胞免疫调节功能缺陷、T 淋巴细胞库调节功能缺陷、NK 细胞功能缺陷、巨噬细胞细胞因子分泌缺陷 (Fan et al., 2004) 以及伤口愈合能力受损。此品系小鼠也缺乏溶血补体 C5。此外,NOD/ShiLtJ 小鼠的听力也严重受损。多种致免疫缺陷突变、细胞因子基因靶向突变以及影响免疫功能的转基因,均已回交至 NOD/ShiLt 近交系背景。
品系建立
NOD 近交小鼠最早由 Shionogi 白内障 (Cataract Shionogi, CTS) 品系小鼠近交繁殖获得,CTS 小鼠来自于远交系 Jcl:ICR 小鼠。繁殖到 F6 代时,取非白内障、高空腹血糖水平小鼠继续与 NOD/Shi 小鼠祖先进行近交。在 F13 代时,从目前的 NON/Shi 品系分离出 NOD 祖先。虽然高空腹血糖水平仍然是后代品系的选择依据,但 F13 及其后代的 NOD 祖先是根据正常空腹血糖水平选择的。1974 年,繁殖到 F20 代时,“血糖正常”品系雌鼠自发出现明显的胰岛素依赖型糖尿病 (insulin-dependent diabetes mellitus, IDDM) 伴胰岛炎症状。选择性育种此糖尿病雌性后代获得了非肥胖型糖尿病 (nonobese diabetic, NOD) 品系。NOD 亚系最初仅限在日本销售,20 世纪 80 年代初才引入澳大利亚和美国销售。1984 年,M. Hattori 博士将 NOD 和 NON 品系从日本京都的一个小鼠种群引进到波士顿的加斯林糖尿病中心。此次引进的繁育对从加斯林糖尿病中心转呈给杰克森实验室的 E Leiter 博士,成为 NOD/ShiLtJ 和 NON/ShiLtJ 生产品系的小鼠来源。
参考文献
精选参考文献
当使用该小鼠品系发表文献时,请引用原始文献,并在材料方法中提供该品系的品系货号:JAX stock#001976
2019

Therapeutic administration of Tregitope-Human Albumin Fusion with Insulin Peptides to promote Antigen-Specific Adaptive Tolerance Induction.

De Groot AS , et al.

PubMed:31695065

MGI:J:281351

Sci Rep 9(1):16103

2017

Complete overview of protein-inactivating sequence variations in 36 sequenced mouse inbred strains.

Timmermans S , et al.

PubMed:28784771

MGI:J:244295

Proc Natl Acad Sci U S A 114(34):9158-9163

2015

Genetic Analysis of Substrain Divergence in Non-Obese Diabetic (NOD) Mice.

Simecek P , et al.

PubMed:25740934

MGI:J:257336

G3 (Bethesda) 5(5):771-5

基因分型和繁育
近似对照
ICR/HaJ                              NOD.129S7(B6)-Rag1tm1Mom/J              
NOD.B10Sn-H2b/J               NOD.Cg-Prkdcscid/J               
小鼠在离乳时经爪垫接种弗氏完全佐剂 (Complete Freund's Adjuvant, CFA) 将延迟糖尿病发病时间,从而延长繁育对寿命。关于弗氏完全佐剂在 NOD 小鼠中应用的讨论,请参阅《现行免疫学方案》(Current Protocols in Immunology) 第 15.9.1-15.9.23 页(参见免疫学方案下方的 PDF 链接)。
繁育策略
同胞兄弟姐妹交配
销售和使用条款

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001976
NOD
代谢研究,免疫研究
参考文献|
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  •  
    精选参考文献
    当使用该小鼠品系发表文献时,请引用原始文献,并在材料方法中提供该品系的品系货号:JAX stock#001976

    2019
    Therapeutic administration of Tregitope-Human Albumin Fusion with Insulin Peptides to promote Antigen-Specific Adaptive Tolerance Induction.
    De Groot AS , et al.
    PubMed:31695065
    MGI:J:281351
    Sci Rep 9(1):16103

    2017
    Complete overview of protein-inactivating sequence variations in 36 sequenced mouse inbred strains.
    Proc Natl Acad Sci U S A 114(34):9158-9163
    PubMed:28784771
    MGI:J:244295
    Sci Rep 9(1):16103

    2015
    Genetic Analysis of Substrain Divergence in Non-Obese Diabetic (NOD) Mice.
    Simecek P , et al.
    PubMed:25740934
    MGI:J:257336
    G3 (Bethesda) 5(5):771-5

    1997
    Initiation of autoimmune diabetes in NOD/Lt mice is MHC class I-dependent.
    Serreze DV , et al.
    PubMed:9103469
    MGI:J:39473
    J Immunol 158(8):3978-86

    1993
    The NOD mouse: A model for analyzing the interplay between heredity and environment in development of autoimmune disease.
    Leiter EH , et al.
    PubMed:
    MGI:J:12784
    ILAR News 35(1):4-14

    1980
    Breeding of a non-obese, diabetic strain of mice.
    Makino S , et al.
    PubMed:6995140
    MGI:J:25411
    Jikken Dobutsu 29(1):1-13

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    其它参考文献

    2016
    Unstable FoxP3+ T regulatory cells in NZW mice.
    Depis F , et al.
    PubMed:26768846
    MGI:J:227903
    Proc Natl Acad Sci U S A 113(5):1345-50

    2011
    Mouse genomic variation and its effect on phenotypes and gene regulation.
    Keane TM , et al.
    PubMed:21921910
    MGI:J:177037
    Nature 477(7364):289-94

    2008
    Social approach and repetitive behavior in eleven inbred mouse strains.
    Moy SS , et al.
    PubMed:18440079
    MGI:J:138681
    Behav Brain Res 191(1):118-29

    2004
    Development of a SNP genotyping panel for genetic monitoring of the laboratory mouse.
    Petkov PM , et al.
    PubMed:15081119
    MGI:J:89298
    Genomics 83(5):902-11

    2004
    Strain distribution pattern of susceptibility to immune-mediated nephritis.
    Xie C , et al.
    PubMed:15067087
    MGI:J:122988
    J Immunol 172(8):5047-55

    2003
    Adenovirus early region 3 antiapoptotic 10.4K, 14.5K, and 14.7K genes decrease the incidence of autoimmune diabetes in NOD mice.
    Pierce MA , et al.
    PubMed:12716741
    MGI:J:83195
    Diabetes 52(5):1119-27

    2002
    During the early prediabetic period in NOD mice, the pathogenic CD8(+) T-cell population comprises multiple antigenic specificities.
    DiLorenzo TP , et al.
    PubMed:12498815
    MGI:J:94192
    Clin Immunol 105(3):332-41

    2001
    Cytotoxic T lymphocyte and cDNA sequence analyses of the MHC class Ib molecule Qa1 in nonobese diabetic mice.
    Chun T , et al.
    PubMed:11685462
    MGI:J:72438
    Immunogenetics 53(6):506-10

    2001
    Reduced oral wound healing in the NOD mouse model for type 1 autoimmune diabetes and its reversal by epidermal growth factor supplementation.
    Nagy A , et al.
    PubMed:11522677
    MGI:J:71049
    Diabetes 50(9):2100-4

    2001
    Autoantibody Patterns in Diabetes-prone NOD Mice and in Standard C57BL/6 Mice.
    Quintana FJ , et al.
    PubMed:11712856
    MGI:J:72893
    J Autoimmun 17(3):191-7

    2001
    Il-12 administration reveals diabetogenic t cells in genetically resistant i-ealpha-transgenic nonobese diabetic mice: resistance to autoimmune diabetes is associated with binding of ealpha-derived peptides to the i-a(g7) molecule.
    Trembleau S , et al.
    PubMed:11564833
    MGI:J:71651
    J Immunol 167(7):4104-14

    2000
    Interferon-gamma receptor signaling is dispensable in the development of autoimmune type 1 diabetes in NOD mice.
    Serreze DV , et al.
    PubMed:11118001
    MGI:J:65986
    Diabetes 49(12):2007-11

    1998
    NOD Mice and Related Strains: Origins, Husbandry and Biology Introduction
    Leiter EH , et al.

    1997
    Apoptosis is increased in a model of diabetes-impaired wound healing in genetically diabetic mice.
    Darby IA , et al.
    PubMed:9076954
    MGI:J:40898
    Int J Biochem Cell Biol 29(1):191-200

    1995
    Studies on the polymorphism of the fifth component of complement in laboratory mice.
    Lynch DM , et al.
    PubMed:8919358
    MGI:J:31912
    Exp Clin Immunogenet 12(4):253-60

    1994
    Prevention of diabetes in the NOD mouse: implications for therapeutic intervention in human disease.
    Bowman MA , et al.
    PubMed:8172643
    MGI:J:17091
    Immunol Today 15(3):115-20

    1994
    Genetic and pathogenic basis of autoimmune diabetes in NOD mice.
    Serreze DV , et al.
    PubMed:7710714
    MGI:J:22216
    Curr Opin Immunol 6(6):900-6

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albino

Related Genotype: A/A

Tyrc/Tyrc