Nonobese diabetic mice and the genetics of diabetes susceptibility

被引：24

作者：

Leiter E.H. ^{[1
]}

机构：

[1] The Jackson Laboratory, Bar Harbor, ME 04609

来源：

Current Diabetes Reports | 2005年 / 5卷 / 2期

基金：

美国国家卫生研究院;

关键词：

Major Histocompatibility Complex; Major Histocompatibility Complex Class; Experimental Allergic Encephalomyelitis; Congenic Strain; Diabetes Susceptibility;

D O I：

10.1007/s11892-005-0042-z

中图分类号：

学科分类号：

摘要：

The nonobese diabetic mouse spontaneously develops an autoimmune, T-cell-mediated type I diabetes (TID). Common and rare alleles both within a diabetogenic major histocompatibility complex (MHC) and multiple non-MHC genes combine to impair normal communication between the innate and acquired immune system, leading to loss of immune tolerance. An understanding of how variable collections of genes interact with each other and with environmental cues offers important insights as to the complexities of TID inheritance in humans. Copyright © 2005 by Current Science Inc.

引用

页码：141 / 148

页数：7

共 55 条

[1]

Zavattari P., Lampis R., Motzo C., Et al., Conditional linkage disequilibrium analysis of a complex disease superlocus, IDDM1 in the HIA region, reveals the presence of independent modifying gene effects influencing the type 1 diabetes risk encoded by the major HLA-DQB1, -DRB1 disease loci, Hum. Mol. Genet., 10, pp. 881-889, (2001)

[2]

Rich S.S., Concannon P., Challenges and strategies for investigating the genetic complexity of common human diseases, Diabetes, 51, SUPPL. 3, (2002)

[3]

Concannon P., Gogolin-Ewens K.J., Hinds D.A., Et al., A second-generation screen of the human genome for susceptibility to insulin-dependent diabetes mellitus, Nat. Genet., 19, pp. 292-296, (1998)

[4]

Ueda H., Howson J.M., Esposito L., Et al., Association of the T-cell regulatory gene CTLA4 with susceptibility to autoimmune disease, Nature, 423, pp. 506-511, (2003)

[5]

Ridgway W.M., The non obese diabetic (NOD) mouse: A unique model for understanding the interaction between genetics and T cell responses, Rev. Endocr. Metab. Disord., 4, pp. 263-269, (2003)

[6]

Choisy-Rossi C.M., Holl T.M., Pierce M.A., Et al., Enhanced pathogenicity of diabetogenic T cells escaping a non-MHC gene-controlled near death experience, J. Immunol., 173, pp. 3791-3800, (2004)

[7]

Serreze D.V., Leiter E.H., Genes and pathways underlying autoimmune diabetes in NOD mice, Molecular Pathology of Insulin-Dependent Diabetes Mellitus, 4, pp. 31-67, (2001)

[8]

Serreze D.V., Holl T.M., Marron M.P., Et al., MHC class II molecules play a role in the selection of autoreactive class I-restricted CD8 T cells that are essential contributors to type 1 diabetes development in nonobese diabetic mice, J. Immunol., 172, pp. 871-879, (2004)

[9]

Hamilton-Williams E.E., Serreze D.V., Charlton B., Et al., Transgenic rescue implicates beta2-microglobulin as a diabetes susceptibility gene in NOD mice, Proc. Natl. Acad. Sci. U. S. A., 98, pp. 11533-11538, (2001)

[10]

Ikegami H., Makino S., The NOD mouse and its related strains, Animal Models of Diabetes A Primer, pp. 43-61, (2001)

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