Analysis of 19 genes for association with type I diabetes in the Type I Diabetes Genetics Consortium families

Howson, Joanna M.M.; Walker, Neil M.; Smyth, Deborah J.; Todd, John A.

doi:10.1038/gene.2009.96

Cited by 85 publications

(67 citation statements)

References 68 publications

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“…The primary HLA associations with T1D are now well established to be with class II genes, specifically those encoding the DR and DQ molecules, as described above. However, alleles at the class I loci A and B loci have also been shown to affect T1D susceptibility independently from class II; in particular, class I alleles appear to play a role in age of onset of T1D (Noble et al 2002Tait et al 2003;Valdes et al 2005;Nejentsev et al 2007;Howson et al 2009b). T1D is believed to result from an initial triggering event, followed by gradual autoimmune destruction of the pancreatic b cells, until the point that the residual b cells are insufficient to meet the insulin demands of the body, leading to hyperglycemia and disease diagnosis.…”

Section: Hla Class Imentioning

confidence: 99%

Genetics of Type 1 Diabetes

Noble¹,

Erlich²

2012

Cold Spring Harbor Perspectives in Medicine

257

157

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Section: Hla Class Imentioning

confidence: 99%

Genetics of Type 1 Diabetes

Noble¹,

Erlich²

2012

Cold Spring Harbor Perspectives in Medicine

257

157

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“…Peripheral B-cells from RA patients have an altered expression of CD86 (Catalan et al, 2010). Associations with CD86 polymorphisms were reported in systemic sclerosis and several cancers (Abdallah et al, 2006;Howson et al, 2009;Landi et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

CTLA-4 and CD86 genetic variants and haplotypes in patients with rheumatoid arthritis in southeastern China

Liu

Jiang²,

Wang³

et al. 2013

Genet. Mol. Res.

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ABSTRACT. The cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) and costimulatory molecule (CD80/CD86) genes are important susceptibility genes associated with autoimmune diseases. CTLA-4 polymorphisms have been found to be associated with various autoimmune diseases. However, the association data are inconsistent for rheumatoid arthritis (RA). We investigated the genetic association of CTLA-4 and CD86 polymorphisms with RA in a Chinese population. Four single nucleotide polymorphisms (SNPs) (rs5742909 and rs231775 in CTLA-4, and rs17281995 and rs1129055 in CD86) were genotyped in 213 patients with RA and 303 healthy controls using polymerase chain reaction-restriction fragment length polymorphism. The genotype and allele distributions of rs5742909 differ significantly between RA patients and controls (P < 0.05) and the dominant model was found to be the best inheritance model. Stratification studies showed that CTLA-4 gene polymorphisms were more significantly associated with rheumatoid factor-negative and anti-cyclic citrullinated peptide-negative subgroups in the southeastern Han Chinese population. We also found that the haplotype of 2 CTLA-4 SNPs showed significant association with the disease (P = 0.0025) with the T-A (OR = 1.88, 95%CI = 1.12-3.15) and T-G (OR = 3.45, 95%CI = 1.10-10.87) haplotypes being observed more frequently in cases than in controls. We failed to find any significant association of the 2 CD86 SNPs with RA. These results indicate that the polymorphisms of CTLA-4 (rs5742909) may be important genetic factors for RA risk in the southeastern Han Chinese population.

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“…The selection criteria for adult patients are year at diagnosis under 35 years and uninterrupted insulin treatment for at least 6 months (Hakonarson et al, 2007). However, despite the wider limit in age at onset in this population, the majority of the patients included are pediatric, as reflected in the mean age at onset (around ten years) found in the published studies (Hakonarson et al, 2008;Howson et al, 2009). …”

Section: The Problem With Age At Diagnosismentioning

confidence: 92%

“…Since 2007, the consortium has published several studies on type 1 diabetes genetics (Erlich et al, 2008;Hakonarson et al, 2008;Howson et al, 2009;Qu et al, 2009) and, although the genome-wide study in which the T1DGC population was genotyped did not include an age-at-onset analysis, this group is lately including age-at-onset analyses in their publications and some of their studies have provided the first evidences of influence of genetics in age at onset of the post-genome wide era (Hakonarson et al, 2008). The selection criteria for adult patients are year at diagnosis under 35 years and uninterrupted insulin treatment for at least 6 months (Hakonarson et al, 2007).…”

Section: The Problem With Age At Diagnosismentioning

confidence: 99%