Type 1A diabetes induced by infection and immunization

被引:22
作者
Robles, DT [1 ]
Eisenbarth, GS [1 ]
机构
[1] Univ Colorado, Hlth Sci Ctr, Barbara Davis Ctr Childhood Diabet, Denver, CO 80262 USA
关键词
D O I
10.1006/jaut.2000.0483
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Type 1A diabetes is an immune mediated disorder that results from progressive destruction of the islet beta -cells in the setting of genetic susceptibility. Both MHC and non-MHC genes contribute to disease with class II HLA molecules major determinants of susceptibility or protection. The presence of multiple anti-islet autoantibodies is associated with a high risk of disease progression, and the first anti-islet autoantibodies may appear as early as the first year of life. Congenital rubella is the only infection clearly associated with the development of type 1A diabetes. With the ability to detect children in the first year of life activating autoimmunity, prospective studies may in the future document additional environmental factors either increasing or decreasing diabetes risk. (C) 2001 Academic Press.
引用
收藏
页码:355 / 362
页数:8
相关论文
共 70 条
[1]   AN AUTOSOMAL LOCUS CAUSING AUTOIMMUNE-DISEASE - AUTOIMMUNE POLYGLANDULAR DISEASE TYPE-I ASSIGNED TO CHROMOSOME-21 [J].
AALTONEN, J ;
BJORSES, P ;
SANDKUIJL, L ;
PERHEENTUPA, J ;
PELTONEN, L .
NATURE GENETICS, 1994, 8 (01) :83-87
[2]   Dual overlapping peptides recognized by insulin peptide B:9-23 T cell receptor AV13S3 T cell clones of the NOD mouse [J].
Abiru, N ;
Wegmann, D ;
Kawasaki, E ;
Gottlieb, P ;
Simone, E ;
Eisenbarth, GS .
JOURNAL OF AUTOIMMUNITY, 2000, 14 (03) :231-237
[3]   The NOD mouse model of type 1 diabetes: As good as it gets? [J].
Atkinson, MA ;
Leiter, EH .
NATURE MEDICINE, 1999, 5 (06) :601-604
[4]   INSULITIS AND DIABETES IN NOD MICE REDUCED BY PROPHYLACTIC INSULIN THERAPY [J].
ATKINSON, MA ;
MACLAREN, NK ;
LUCHETTA, R .
DIABETES, 1990, 39 (08) :933-937
[5]   CELLULAR-IMMUNITY TO A DETERMINANT COMMON TO GLUTAMATE-DECARBOXYLASE AND COXSACKIE-VIRUS IN INSULIN-DEPENDENT DIABETES [J].
ATKINSON, MA ;
BOWMAN, MA ;
CAMPBELL, L ;
DARROW, BL ;
KAUFMAN, DL ;
MACLAREN, NK .
JOURNAL OF CLINICAL INVESTIGATION, 1994, 94 (05) :2125-2129
[6]  
Bach JF, 1999, CONT ENDOCRINOL, V15, P293
[7]   Mutations in the AIRE gene:: Effects on subcellular location and transactivation function of the autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy protein [J].
Björses, P ;
Halonen, M ;
Palvimo, JJ ;
Kolmer, M ;
Aaltonen, J ;
Ellonen, P ;
Perheentupa, J ;
Ulmanen, I ;
Peltonen, L .
AMERICAN JOURNAL OF HUMAN GENETICS, 2000, 66 (02) :378-392
[8]   Localization of the APECED protein in distinct nuclear structures [J].
Björses, P ;
Pelto-Huikko, M ;
Kaukonen, J ;
Aaltonen, J ;
Peltonen, L ;
Ulmanen, I .
HUMAN MOLECULAR GENETICS, 1999, 8 (02) :259-266
[9]  
Bjorses P, 1996, AM J HUM GENET, V59, P879
[10]   THE SWEDISH CHILDHOOD DIABETES STUDY - VACCINATIONS AND INFECTIONS AS RISK DETERMINANTS FOR DIABETES IN CHILDHOOD [J].
BLOM, L ;
NYSTROM, L ;
DAHLQUIST, G .
DIABETOLOGIA, 1991, 34 (03) :176-181