1. Association of HLA-DQ alleles with the presence of an anti-β₂-glycoprotein I antibody in patients with recurrent miscarriage.
- Author
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Chen X, Liang PY, Li GG, Diao LH, Liu CC, Huang CY, Wu TH, Xu J, and Zeng Y
- Subjects
- Abortion, Habitual blood, Abortion, Habitual immunology, Abortion, Habitual pathology, Adult, Autoimmune Diseases blood, Autoimmune Diseases immunology, Autoimmune Diseases pathology, Female, Gene Expression, Gene Frequency, Genetic Predisposition to Disease, HLA-DQ alpha-Chains genetics, HLA-DQ beta-Chains genetics, Histocompatibility Testing, Humans, Immunoglobulin G blood, Immunoglobulin M blood, Pregnancy, beta 2-Glycoprotein I blood, beta 2-Glycoprotein I immunology, Abortion, Habitual genetics, Alleles, Autoantibodies blood, Autoimmune Diseases genetics, HLA-DQ alpha-Chains immunology, HLA-DQ beta-Chains immunology
- Abstract
Immunogenetic studies have suggested that autoantibody production is commonly associated with particular human leukocyte antigens (HLA) class II genotypes in certain autoimmune diseases. The objective of this study was to investigate whether the production of anti-β2-glycoprotein I antibody (aβ2GPI) was associated with particular HLA-DQ alleles in patients with recurrent miscarriage (RM). The HLA-DQ genotypes in 126 patients with RM were determined using the polymerase chain reaction-sequence-specific primer method. Both the IgG and IgM isotypes of aβ2GPI were measured via enzyme-linked immunosorbent assay. Positive results for either IgG or IgM on two occasions within an interval of 12 weeks were defined as antiphospholipid antibody-positive. The frequencies of the HLA-DQA1*01:02 [odds ratio (OR) 3.4, 95% confidence interval (CI) 1.6-7.0, Pc = 0.018] and HLA-DQB1*02:01 alleles (OR 4.6, 95% CI 2.1-10.2, Pc = 9.18 × 10(-4)) were significantly increased in aβ2GPI-positive RM patients compared with aβ2GPI-negative RM patients. These results suggest that the HLA-DQA1*0102 and HLA-DQB1*0201 alleles may be involved in the production of aβ2GPI in RM patients., (© 2015 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)
- Published
- 2016
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