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NOD.Cg-Prkdcscid/J
品系货号：001303 ｜ 通用名称：NOD scid
又名： NOD SCID
摘要
此品系为严重联合免疫缺陷自发突变 Prkdcscid 纯合小鼠，通常称为 scid 小鼠，表现为功能性 T 细胞和 B 细胞缺失、淋巴细胞减少症、低丙种球蛋白血症，但造血微环境正常。Prkdcscid 小鼠可以接受同种异体和异种异体移植物，因此是细胞转移实验的理想模型。总体而言，NOD/ShiLtSz 遗传背景下的 Prkdcscid渗漏表达较低。
品系特点
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品系详情
此品系为严重联合免疫缺陷自发突变 Prkdcscid 纯合小鼠，通常称为 scid 小鼠，表现为功能性 T 细胞和 B 细胞缺失、淋巴细胞减少症、低丙种球蛋白血症，但造血微环境正常。抗原呈递细胞、髓系细胞和 NK 细胞的正常功能具有品系依赖性。scid 小鼠携带 DNA 修复缺陷和编码淋巴细胞中抗原特异性受体的基因重排缺陷。大多数纯合子未检出 IgM、IgG1、IgG2a、IgG2b、IgG3 或 IgA。胸腺、淋巴结和脾脏滤泡中几乎没有淋巴细胞。scid 小鼠可以接受同种异体和异种异体移植物，因此是细胞转移实验的理想模型。
有些 scid 小鼠会自发出现局部免疫反应。血清 Ig 水平高于 1 ug/ml 的 scid 小鼠被视为“渗漏表达”。scid渗漏具有高度品系依赖性、随周龄增加，在非 SPF 条件下笼养的小鼠中比例更高。总体而言，scid 渗漏率在 C57BL/6J 和 BALB/cBy 遗传背景中较高，在 C3H/HeJ 背景中较低，在 NOD/ShiLtSz 背景中更低。NOD/ShiLtSz-Prkdcscid 小鼠终生不患胰岛炎和糖尿病，可作为NOD/ShiLtJ 小鼠（品系货号 001976）的无糖尿病对照。不过，其胸腺淋巴瘤发病率较高，在无特定病原条件下（SPF），寿命通常仅限于 8.5 月龄。NOD.CB17-Prkdcscid/J 小鼠除可用作异体移植的理想宿主外，还有可用于研究T 细胞亚群在自身免疫性糖尿病中的作用，同时也可作为无胰岛炎胰岛细胞的来源。
品系建立
Prkdcscid 突变是在宾夕法尼亚州费城癌症研究所饲养的 BALB/c-Ighb (CB-17) 小鼠种群中自发产生的突变。将 Prkdcscid 突变按照如下描述回交至 NOD/ShiLtSz 背景中：使 NOD/ShiLtSz 雌鼠与 C.B-17-Prkdcscid 雄鼠交配；使 F1/N1 和随后数代 Prkdcscid/+ 雄鼠后代与 NOD/ShiLtSz 雌鼠交配，总共与 NOD/ShiLtSz 回交 10 代；在 N10 代时，通过兄弟姊妹近亲交配得到 Prkdcscid 纯合小鼠。
参考文献
精选参考文献
如果研究中使用了NOD scid小鼠品系，请在发表文章时请引用原始文献并在材料和方法部分提及JAX品系号001303。
1998
Xenotransplantation of human lymphoid malignancies is optimized in mice with multiple immunologic defects.
Hudson WA , et al.
1996
Identification of a nonsense mutation in the carboxyl-terminal region of DNA-dependent protein kinase catalytic subunit in the scid mouse.
Blunt T , et al.
1995
Defective DNA-dependent protein kinase activity is linked to V(D)J recombination and DNA repair defects associated with the murine scid mutation.
Blunt T , et al.
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001303
NOD scid
肿瘤免疫，癌症研究，免疫相关研究，糖尿病及肥胖
参考文献|
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精选参考文献如果研究中使用了NOD scid小鼠品系，请在发表文章时请引用原始文献并在材料和方法部分提及JAX品系号001303。
1998Xenotransplantation of human lymphoid malignancies is optimized in mice with multiple immunologic defects.
Hudson WA , et al.
1996Identification of a nonsense mutation in the carboxyl-terminal region of DNA-dependent protein kinase catalytic subunit in the scid mouse.
Blunt T , et al.
1995Defective DNA-dependent protein kinase activity is linked to V(D)J recombination and DNA repair defects associated with the murine scid mutation.
Blunt T , et al.
1995Emv30null NOD-scid mice. An improved host for adoptive transfer of autoimmune diabetes and growth of human lymphohematopoietic cells.
Serreze DV , et al.
1995Multiple defects in innate and adaptive immunologic function in NOD/LtSz-scid mice.
Shultz LD , et al.
1993Adoptive transfer of diabetes into immunodeficient NOD-scid/scid mice. Relative contributions of CD4+ and CD8+ T-cells from diabetic versus prediabetic NOD.NON-Thy-1a donors.
Christianson SW , et al.
1993High frequency of thymic ectopy in thyroids from autoimmune prone nonobese diabetic female mice.
Many MC , et al.
1993Strain-dependent leakiness of mice with severe combined immune deficiency.
Nonoyama S , et al.
1992The nonobese diabetic scid mouse: model for spontaneous thymomagenesis associated with immunodeficiency.
Prochazka M , et al.
1988The scid mouse mutant.
Bosma M , et al. -
其它参考文献
2014NOD-scidIl2rg (tm1Wjl) and NOD-Rag1 (null) Il2rg (tm1Wjl) : a model for stromal cell-tumor cell interaction for human colon cancer.
Maykel J , et al.
2004T-cell receptor transgenic response to an endogenous polymorphic autoantigen determines susceptibility to diabetes.
Pauza ME , et al.
2003Tim-3 inhibits T helper type 1-mediated auto- and alloimmune responses and promotes immunological tolerance.
Sanchez-Fueyo A , et al.
2003Contribution of Fas to diabetes development.
Savinov AY , et al.
2003Non-obese diabetic mice rapidly develop dramatic sympathetic neuritic dystrophy: a new experimental model of diabetic autonomic neuropathy.
Schmidt RE , et al.
2002Indoleamine 2,3-dioxygenase expression in transplanted NOD Islets prolongs graft survival after adoptive transfer of diabetogenic splenocytes.
Alexander AM , et al.
2002Susceptibility to lymphoid neoplasia in immunodeficient strains of nonobese diabetic mice.
Chiu PP , et al.
2002Congenic mapping of the diabetogenic locus Idd4 to a 5.2-cM region of chromosome 11 in NOD mice: identification of two potential candidate subloci.
Grattan M , et al.
2002Elimination of maternally transmitted autoantibodies prevents diabetes in nonobese diabetic mice.
Greeley SA , et al.
2002Regulation of diabetes development by regulatory T cells in pancreatic islet antigen-specific TCR transgenic nonobese diabetic mice.
Kanagawa O , et al.
2001Previously undetected human hematopoietic cell populations with short-term repopulating activity selectively engraft NOD/SCID-beta2 microglobulin-null mice.
Glimm H , et al.
2001Human homologues of Delta-1 and Delta-4 function as mitogenic regulators of primitive human hematopoietic cells.
Karanu FN , et al.
2001Altered myelopoiesis and the development of acute myeloid leukemia in transgenic mice overexpressing cyclin A1.
Liao C , et al.
2001Genetic interactions between ATM and the nonhomologous end-joining factors in genomic stability and development.
Sekiguchi J , et al.
2001Il-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.
2000Porcine stem cell engraftment and seeding of murine thymus with class II+ cells in mice expressing porcine cytokines: toward tolerance induction across discordant xenogeneic barriers.
Chen AM , et al.
2000Thymic and postthymic regulation of diabetogenic CD8 T cell development in TCR transgenic nonobese diabetic (NOD) mice.
Kanagawa O , et al.
1993Granulosa cell tumorigenesis in genetically hypogonadal-immunodeficient mice grafted with ovaries from tumor-susceptible donors.
Beamer WG , et al.
1985Severe combined immunodeficiency (SCID) in the mouse. Pathology, reconstitution, neoplasms.
Custer RP , et al.
1984Functional status of cells from lymphoid and myeloid tissues in mice with severe combined immunodeficiency disease.
Dorshkind K , et al.
