Central nervous system malformations in the Kraków region. II. Case control studies on the human leukocyte antigen genotype and haplotype frequenciess

1984 ◽  
Vol 18 (1) ◽  
pp. 89-97 ◽  
Author(s):  
Jacek J. Pietrzyk ◽  
Gabriel Turowski ◽  
Bogdan Róźański
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Human Leukocyte Antigen ◽  
Human Leukocyte ◽  
Case Control ◽  
Case Control Studies ◽  
Leukocyte Antigen ◽  
Region Ii ◽  
Human Leukocyte Antigen Genotype

The influence of human leukocyte antigen-DRB1*15:01 and its interaction with smoking in MS development is dependent on DQA1*01:01 status

2019 ◽  
Vol 26 (13) ◽  
pp. 1638-1646 ◽  
Author(s):  
Anna Karin Hedström ◽  
Ola Hössjer ◽  
Jan Hillert ◽  
Pernilla Stridh ◽  
Ingrid Kockum ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Human Leukocyte Antigen ◽  
Human Leukocyte ◽  
Population Based ◽  
Case Control ◽  
Case Control Studies ◽  
Swedish Population ◽  
Leukocyte Antigen ◽  
Smoking Interaction ◽  
Additive Scale

Background: HLA-DRB1*15:01, absence of HLA-A*02:01, and smoking interact to increase multiple sclerosis (MS) risk. Objective: To analyze whether MS-associated human leukocyte antigen (HLA) alleles, apart from DRB1*15:01 and absence of A*02:01, interact with smoking in MS development, and to explore whether the established HLA-smoking interaction is affected by the DQA1*01:01 allele, which confers a protective effect only in the presence of DRB1*15:01. Methods: In two Swedish population-based case–control studies (5838 cases, 5412 controls), subjects with different genotypes and smoking habits were compared regarding MS risk, by calculating odds ratios with 95% confidence intervals employing logistic regression. Interaction on the additive scale between different genotypes and smoking was evaluated. Results: The DRB1*08:01 allele interacted with smoking to increase MS risk. The interaction between DRB1*15:01 and both the absence of A*02:01 and smoking was confined to DQA1*01:01 negative subjects, whereas no interactions occurred among DQA1*01:01 positive subjects. Conclusion: Multifaceted interactions take place between different class II alleles and smoking in MS development. The influence of DRB1*15:01 and its interaction with the absence of A*02:01 and smoking is dependent on DQA1*01:01 status which may be due to differences in the responding T-cell repertoires.

A Systematic Review and Meta-Analysis of HLA-Class-II Associations in Patients with IgG4 Autoimmunity

2021 ◽  
Author(s):  
Anja Panhuber ◽  
Giovanni Lamorte ◽  
Veronica Bruno ◽  
Hakan Cetin ◽  
Wolfgang Bauer ◽  
...  
Keyword(s):  
Systematic Review ◽  
Autoimmune Diseases ◽  
Genetic Risk ◽  
Meta Analysis ◽  
Human Leukocyte ◽  
Pemphigus Vulgaris ◽  
Case Control ◽  
Case Control Studies ◽  
Leukocyte Antigen ◽  
Susceptibility Factors

Abstract Autoimmune diseases caused by pathogenic IgG4 subclass autoantibodies (IgG4-AID) include diseases like MuSK myasthenia gravis, pemphigus vulgaris or thrombotic thrombocytopenic purpura. Their etiology is still unknown. Polymorphisms in the human leukocyte antigen (HLA) gene locus, particularly in HLA-DRB1, are known genetic susceptibility factors for autoimmune diseases. We hypothesized a similar role for HLA polymorphisms in IgG4-AID and conducted a systematic review and meta-analysis with case-control studies on IgG4-AID based on MOOSE/ HuGENet guidelines. Genotype (G) and allele (A) frequencies of HLA-DQB1*05 (G: OR 3.8; 95% CI 2.44-5.9; p < 0.00001; A: OR 2.54; 95% CI 1.82-3.55; p < 0.00001) and HLA-DRB1*14 (G: OR 4.31; 95% CI 2.82-6.59; p < 0.00001; A: OR 4.78; 95% CI 3.52-6.49; p < 0.00001) and the HLA-DRB1*14-DQB1*05 haplotype (OR 6.3; 95% CI 3.28-12.09; p < 0.00001 / OR 4.98; 95% CI 3.8-6.53; p < 0.00001) were increased while HLA-DRB1*13 (G: OR 0.48; 95% CI 0.34-0.68; p < 0.0001; A: OR 0.46; 95% CI 0.34-0.62; p < 0.00001) was decreased in IgG4-AID patients. In conclusion, the HLA-DQB1*05, HLA-DRB1*14 alleles and the HLA-DQB1*05-DRB1*14 haplotype could be genetic risk factors that predispose for the production of pathogenic IgG4 autoantibodies and the HLA-DRB1*13 allele may protect from IgG4 autoimmunity.

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