Comprehensive Analysis of the HLA Class I and the HLA class II Alleles in Patients with Takayasu Arteritis: Relationship with Clinical Patterns and Prognosis
نویسندگان
1 Clinic of Allergy and Immunology, Clinical Center of Serbia, Belgrade, Serbia, Faculty of Medicine, University of Belgrade, Belgrade, Serbia.
2 Tissue Typing Department, Blood Transfusion Institute of Serbia, Belgrade, Serbia.
3 Clinic of Allergy and Immunology, Clinical Center of Serbia, Belgrade, Serbia, Faculty of Medicine, University of Belgrade, Belgrade, Serbia.
4 Clinic of Allergy and Immunology, Clinical Center of Serbia, Belgrade, Serbia, Faculty of Medicine, University of Belgrade, Belgrade, Serbia.
5 Clinic of Allergy and Immunology, Clinical Center of Serbia, Belgrade, Serbia, Faculty of Medicine, University of Belgrade, Belgrade, Serbia.
6 Institute of Microbiology and Immunology, Faculty of Medicine, University of Belgrade, Belgrade, Serbia.
7 Department of Pathophysiology, Faculty of Medicine, University of Belgrade, Belgrade, Serbia.
8 Clinic of Allergy and Immunology Clinical Center of Serbia, Belgrade, Serbia.
9 Clinic of Allergy and Immunology, Clinical Center of Serbia, Belgrade, Serbia, Faculty of Medicine, University of Belgrade, Belgrade, Serbia.
10 Clinic of Allergy and Immunology, Clinical Center of Serbia, Belgrade, Serbia, Faculty of Medicine, University of Belgrade, Belgrade, Serbia.
doi
10.22034/iji.2021.88846.1911چکیده
Background: Takayasu arteritis (TA) is a systemic vasculitis, affecting mainly the aorta and its branches. Objective: To analyze the HLA class I and class II alleles in patients with TA and explore their relationship with clinical and demographic characteristics, and potential significance in prognosis. Methods: Twenty-five, unrelated TA patients were genotyped for HLA-A, HLA-B, HLA-C, HLA-DRB1, and the HLA-DQB1 loci. The frequencies of the HLA-A, HLA-B, and the HLA-DRB1 were compared with a control group of 1992, while the HLA-C and the HLA-DQB1 were compared with a group of 159 healthy, unrelated individuals. Results: Among TA patients, 5/25 (20%) were identified as the HLA-B*52 carriers. There was a significant difference in the HLA-B*52 allele frequency in the TA patients (10%) compared with the healthy controls (1.2%). Moreover, presence of the HLA-B*52 was associated with significantly earlier disease onset, more severe clinical presentations, and a poorer response to treatment. The HLA-C*03 was detected in 32% of patients and was present exclusively in those with a clinically mild form of the TA, indicating a putative protective effect. Conclusion: These findings indicate that the HLA-B*52 allele contributes to a higher susceptibility to the TA whereas the HLA-C*03, can be a protective factor in the TA.
