DQB1*06 subtyping was available for the Dutch families, and DRB1*04 subtyping was available for all populations. We, therefore, compared the diff-erence in risk of haplotypes in a DRB1*0401-DQB1* 0302-positive genotype relative to the DRB1*03-DQB1* 02-positive genotype with the difference in risk of DRB1* 01-DQB1*05/DRB1*0401-DQB1*0302 vs the DRB1*01-DQB1*05/DRB1*03-DQB1*02 genotype (Table 4). Whether the type 1 diabetes HLA class II associations reflect thymic-positive selection of autoreactive T-cells (susceptible HLA) or the deletion (negative selection) of autoreactive T-cells (protective HLA), preferential presentation of diabetogenic peptides, or alternative immunological mechanisms remains uncertain. HLA association in type 1 diabetes among patients not carrying high-risk DR3-DQ2 or DR4-DQ8 haplotypes. This Asian protective haplotype with DQB1 Val-57 represents an exception to the “general rule” that protective haplotypes encode DQB1 Asp-57. In keeping with earlier findings, we observed that 12.2% of the children with newly diagnosed type 1 diabetes had at least one affected first-degree relative (8–11). The type 1 diabetes risk for the protective DRB1*1301-DQA1*0103-DQB1*0603 (OR 0.13 [95% CI 0.07–0.26]) and the moderately predisposing/neutral DRB1*1302-DQA1*0102-DQB1*0604 haplotype (0.87 [0.49–1.52]) is significantly different. Children born during famine in Holland (survivors of ‘the Dutch Hunger Winter’) were found to have significantly higher 2-h plasma glucose concentrations44. To aid in the search for additional type 1 diabetes genes within and outside the HLA region, an international collaboration (the Type 1 Diabetes Genetics Consortium) has collected and is continuing to collect a large number of type 1 diabetic families (multiplex and simplex) from various populations (20).
Only the first child from any family to be diagnosed with diabetes and registered was included as an index case. HLA DR-DQ haplotypes were determined by familial transmission.
The major genetic determinants of type 1 diabetes are alleles at the HLA-DRB1 and DQB1 loci, with both susceptible and protective DR-DQ haplotypes present in all human populations. A majority of the subjects were male (846 of 1,488, 56.9%), and 80.6% (1,200 of 1488) had at least one biological sibling. 894. β-Cell autoimmunity, metabolic decompensation at diagnosis, and HLA genetics were compared in children with familial or sporadic type 1 diabetes. Significant susceptibility was also found for DRB1*0401-DQB1*0302/DRB1*08-DQB1*04 (RTP=17.4), DRB1* 0401-DQB1*0302/DRB1*01-DQB1*05 (RTP=8.8), DRB1* 0401-DQB1*0302/DRB1*13-DQB1*06 (RTP=8.1), DRB1* 0401-DQB1*0302/DRB1*07-DQB1*02 (RTP=6.1), and DRB1*0401-DQB1*0302/DRB1*0401-DQB1*0301 (RTP=5.2). The increased risk of DR3/4-DQB1*0302 heterozygotes relative to DR3/3 and DR4/4 genotypes has led to the hypothesis that the trans-complementing DQ heterodimers are more effective in presenting diabetogenic epitopes to T-cells (44,47). Overall, this analysis confirms susceptible and protective haplotypes reported in many previous studies, with major high-risk haplotypes DRB1* 03-DQB1*02, DRB1*0401-DQB1*0302, and protective haplotypes DRB1*11-DQB1*0301, DRB1*14-DQB1*05, DRB1*07-DQB1*09, DRB1*0407-DQB1*0301, and DRB1*15-DQB1*06 (Table 2).
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