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- Title
HLA Class I Association With Autoimmune Diabetes in Chinese People: Distinct Implications in Classic Type 1 Diabetes and LADA.
- Authors
Ying Xia; Yan Chen; Xia Li; Shuoming Luo; Jian Lin; Gan Huang; Yang Xiao; Zhiying Chen; Zhiguo Xie; Zhiguang Zhou
- Abstract
Context: We aimed to investigate whether human leukocyte antigen (HLA) Class I loci differentially modulated the risk for and clinical features of Chinese people with classic type 1 diabetes (T1D) and latent autoimmune diabetes in adults (LADA). Methods: In this case-control study, genotypes of HLA-A, -B, -C, -DRB1, -DQA1, and -DQB1 loci were obtained from 1067 cases with classic T1D, 1062 cases with LADA, and 1107 normal controls using next-generation sequencing. Results: Despite 4 alleles shared between classic T1D and LADA (protective: A*02:07 and B*46:01; susceptible: B*54:01 and C*08:01), 7 Class I alleles conferred risk exclusively for classic T1D (A*24:02, B*15:02, B*15:18, B*39:01, B*40:06, B*48:01, and C*07:02) whereas only A*02:01 was an additional risk factor for LADA. Class I alleles affected a wide spectrum of T1D clinical features, including positive rate of protein tyrosine phosphatase autoantibody and zinc transporter 8 autoantibody (A*24:02), C-peptide levels (A*24:02), and age at diagnosis (B*46:01, C*01:02, B*15:02, C*07:02, and C*08:01). By contrast, except for the detrimental effect of C*08:01 on C-peptide concentrations in LADA, no other Class I associations with clinical characteristics of LADA could be reported. The addition of Class I alleles refined the risk model consisting only of DR-DQ data in classic T1D while the overall predictive value of the LADA risk model comprising both Class I and II information was relatively low. Conclusion: The attenuated HLA Class I susceptibility to LADA was indicative of a less deleterious immunogenetic nature compared with classic T1D. These autoimmune diabetes-related Class I variants might serve as additional markers in future screening among Chinese people.
- Publication
Journal of Clinical Endocrinology & Metabolism, 2023, Vol 108, Issue 7, pe404
- ISSN
0021-972X
- Publication type
Article
- DOI
10.1210/clinem/dgad006