The use of Idd congenic mice to identify checkpoints of peripheral tolerance to islet antigen

Annals of the New York Academy of Sciences

Volumn 1103, Issue , 2007, Pages 118-127

  Hamilton Williams, Emma E ^a   Martinez, Xavier ^a   Lyman, Michael ^a   Hunter, Kara ^b   Wicker, Linda S ^b   Sherman, Linda A ^a  

^a SCRIPPS RESEARCH INSTITUTE   (United States)

^b UNIVERSITY OF CAMBRIDGE   (United Kingdom)

Author keywords

Autoimmunity; CD8 T lymphocytes; NOD mouse; Type 1 diabetes

Indexed keywords

ANTIGEN;

ALLELE; ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ARTICLE; AUTOIMMUNITY; CD4+ T LYMPHOCYTE; CD8+ T LYMPHOCYTE; CELL TYPE; CONGENIC STRAIN; CONTROLLED STUDY; FEMALE; GENE LOCUS; GENETIC SUSCEPTIBILITY; INSULIN DEPENDENT DIABETES MELLITUS; LYMPH NODE; MOUSE; MOUSE STRAIN; NONHUMAN; NONOBESE DIABETIC MOUSE; PANCREAS; PANCREAS ISLET; T LYMPHOCYTE;

MUS;

EID: 34249067952     PISSN: 00778923     EISSN: 17496632     Source Type: Book Series    
DOI: 10.1196/annals.1394.003     Document Type: Article

References (21)

1. KURTS, C. et al. 1997. Class I-restricted cross-presentation of exogenous self-antigens leads to deletion of autoreactive CD8(+) T cells. J. Exp. Med. 186: 239-245.
2. + T cell tolerance to peripherally expressed antigens. J. Immunol. 163: 723-727.
3. WICKER, L.S. et al. 1987. Genetic control of diabetes and insulitis in the nonobese diabetic (NOD) mouse. J. Exp. Med. 165: 1639-1654.
4. MAIER, L.M. & L.S. WICKER. 2005. Genetic susceptibility to type 1 diabetes. Curr. Opin. Immunol. 17: 601-608.
5. PODOLIN, P.L., et al. 2000. Differential glycosylation of interleukin 2: the molecular basis for the NOD Idd3 type 1 diabetes gene? Cytokine 12: 477-482.
6. WICKER, L.S. et al. 2004. Fine mapping, gene content, comparative sequencing, and expression analyses support Ctla4 and Nramp1 as candidates for Idd5.1 and Idd5.2 in the nonobese diabetic mouse. J. Immunol. 173: 164-173.
7. KISSLER, S. et al. 2006. In vivo RNA interference demonstrates a role for Nramp1 in modifying susceptibility to type 1 diabetes. Nat. Genet. 38: 479-483.
8. ROBLES, D.T. et al. 2003. Insulin autoantibodies are associated with islet inflammation but not always related to diabetes progression in NOD congenic mice. Diabetes 52: 882-886.
9. LYONS, P.A. et al. 2000. The NOD Idd9 genetic interval influences the pathogenicity of insulitis and contains molecular variants of Cd30, Tnfr2, and Cd137. Immunity 13: 107-115.
10. + T-cells from diabetic versus prediabetic NOD.NON-Thy-1a donors. Diabetes. 42: 44-55.
11. KATZ, J., C. BENOIST & D. MATHIS. 1993. Major histocompatibility complex class I molecules are required for the development of insulitis in non-obese diabetic mice. Eur J. Immunol. 23: 3358-3360.
12. LESAGE, S., et al. 2002. Failure to censor forbidden clones of CD4 T cells in autoimmune diabetes. J. Exp. Med. 196: 1175-1188.
13. LISTON, A. et al. 2004. Generalized resistance to thymic deletion in the NOD mouse; a polygenic trait characterized by defective induction of Bim. Immunity 21: 817-830.
14. TISCH, R. et al. 1993. Immune response to glutamic acid decarboxylase correlates with insulitis in non-obese diabetic mice. Nature 366: 72-75.
15. KAUFMAN, D.L. et al. 1993. Spontaneous loss of T-cell tolerance to glutamic acid decarboxylase in murine insulin-dependent diabetes [see comments]. Nature 366: 69-72.
16. + T cells. Eur. J. Immunol. 22: 1013-1022.
17. + T cell peripheral tolerance in nonobese diabetic mice. J. Immunol. 167: 1112-1117.
18. + T cell tolerance in nonobese diabetic mice is restored by insulin-dependent diabetes resistance alleles. J. Immunol. 175: 1677-1685.
19. + T cells from nonobese diabetic mice use highly homologous T cell receptor alpha-chain CDR3 sequences. J. Immunol. 154: 2494-2503.
20. DILORENZO, T.P. et al. 1998. Major histocompatibility complex class I-restricted T cells are required for all but the end stages of diabetes development in nonobese diabetic mice and use a prevalent T cell receptor alpha chain gene rearrangement. Proc. Natl. Acad. Sci. USA 95: 12538-12543.
21. HILL, N.J. et al. 2000. NOD Idd5 locus controls insulitis and diabetes and overlaps the orthologous CTLA4/IDDM12 and NRAMP1 loci in humans. Diabetes 49: 1744-1747.