HLA antigens and age at diagnosis of insulin-dependent diabetes mellitus
References (33)
- et al.
Factors predicting residual beta cell function in the first year after diagnosis of childhood type 1 diabetes
Diabetes Res Clin Pract
(1991) - et al.
Overview: the major histocompatibility complex and insulin dependent diabetes mellitus: genetics of diabetes
Baillieres Clin Endocrinol Metab
(1991) T cell-defined HLA epitopes and T cell receptor polymorphism in insulin-dependent diabetes mellitus
- et al.
Evidence for a long prediabetic period in type 1 (insulin-dependent) diabetes mellitus
Lancet
(1981) Islet cell antigens in insulin-dependent diabetes: Pandora's box revisited
Immunol Today
(1992)- et al.
Antibodies to glutamic acid decarboxylase in at-risk and clinical insulin-dependent diabetic subjects: relationship to age, sex and islet cell antibody status and temporal profile
J Autoimmun
(1994) - et al.
Type 1 diabetes: immunopathology and immunotherapy
Adv Endocrinol Metab
(1990) - et al.
Incidence of diabetes mellitus by clinical type
Diabetes Care
(1983) - et al.
Trends in the prevalence and incidence of diabetes: insulindependent diabetes mellitus in childhood
WHO Stat Quant
(1988) - et al.
Islet cell antibodies identify latent type 1 diabetes in patients aged 35–75 years at diagnosis
Diabetes
(1986)
Juvenile diabetes mellitus: HLA antigen frequencies dependent on the age of onset of the disease
J Immunogenet
An analysis of epidemiological data in HLA typed diabetic children
Diabetologia
DR3 is associated with a more slowly progressive form of type 1 (insulin-dependent) diabetes
Diabetologia
HLA associations in insulin-dependent diabetes: search for heterogeneity in different groups of patients from a homogeneous population
Tissue Antigens
Two distinct HLA-DR3 haplotypes are associated with age-related heterogeneity in type 1 (insulin-dependent) diabetes
Diabetologia
Age-dependent HLA genetic heterogeneity of type 1 insulindependent diabetes mellitus
J Clin Invest
Cited by (76)
Prevention of autoimmune disease: The type 1 diabetes paradigm
2019, The Autoimmune DiseasesPrevention of Autoimmune Disease: The Type 1 Diabetes Paradigm
2013, The Autoimmune Diseases: Fifth EditionTumor necrosis factor-associated susceptibility to type 1 diabetes is caused by linkage disequilibrium with HLA-DR3 haplotypes
2012, Human ImmunologyCitation Excerpt :It is interesting to note that the B8–DR3 haplotypes alone were associated with late age of onset of T1D (10–20 years, 40.3%, and >20 years, 35.3%, compared with <10 years, 18.9%) in the Indian population. A similar study in Caucasians reported that the frequency of the HLA-A1–B8–DR3 haplotypes was increased in patients ≥31 years of age at diagnosis, whereas A30–B18–DR3 occurred primarily in the ≤6-year age group and B62–DR4 in those with disease at onset at ≥12 years [68]. Because the B8–DR3 haplotypes differ at several loci between Caucasians and North Indians, including polymorphisms TNF −308 and TNFa genes, the delayed onset of the disease cannot be attributed only to the TNF block of the B8–DR3 haplotypes and might be influenced by other factors.
Diabetes related autoimmunity in gestational diabetes mellitus: Is it important?
2009, Nutrition, Metabolism and Cardiovascular DiseasesCitation Excerpt :HLA typing is useful in assessing the risk of type 1 diabetes in relatives of type 1 diabetic patients. The DRB1*03,04DQBI*;0201,0302 (DR3,4-DQ2,8) sequence coincides with relatives having a more than 20-fold risk of developing diabetes and is associated with an earlier age at diagnosis [11]. The other characteristic sequences, such as DRB1*04,04; DQB1*0302,0302(DR4,4-DQ8,8), DRB1*03,03; DQB1*0302,Y(DR3,3-DQ8,Y),DRB1*04,03; DQB1*0302,Y(DR4,X-DQ8,Y) and DRB1*03,X, correlate with a lower risk of developing type 1 diabetes.
Searching for Additional Disease Loci in a Genomic Region
2008, Advances in GeneticsCitation Excerpt :For an additive (dominant) model, most patients are expected to be heterozygous rather than homozygous for the associated marker allele. Also, additive expectations continue to hold if we additionally allow for sporadic cases when the marker locus is itself the disease causative agent, for example, HLA‐B27 and ankylosing spondilitis (Thomson, 1983). Expectations for multiple alleles are easily obtained allowing tests of mode of inheritance (Thomson, 1993, 1995a); however, the simple method of moments estimate for the additive model can give problems with multiple alleles if the mode of inheritance is not close to additive.
Increased HLA class II risk is associated with a more aggressive presentation of clinical type 1 diabetes
2023, Acta Paediatrica, International Journal of Paediatrics