%0 Journal Article
%T Takayasu's arteritis is associated with HLA-B*52, but not with HLA-B*51, in Turkey
%A Ziver Sahin
%A Muge B£¿cakc£¿gil
%A Kenan Aksu
%A Sevil Kamali
%A Servet Akar
%A Fatos Onen
%A Omer Karadag
%A Zeynep Ozbalkan
%A Askin Ates
%A Huseyin TE Ozer
%A Vuslat Yilmaz
%A Emire Seyahi
%A Mehmet A Ozturk
%A Ayse Cefle
%A Veli Cobankara
%A A Mesut Onat
%A Ercan Tunc
%A Nursen D¨¹zg¨¹n
%A Sibel Z Aydin
%A Neslihan Yilmaz
%A £¿zzet Fresko
%A Yasar Karaaslan
%A Sedat Kiraz
%A Nurullah Akkoc
%A Murat Inanc
%A Gokhan Keser
%A F Aytul Uyar
%A Haner Direskeneli
%A G¨¹her Saruhan-Direskeneli
%A the Turkish Takayasu Study Group
%J Arthritis Research & Therapy
%D 2012
%I BioMed Central
%R 10.1186/ar3730
%X TAK patients (n = 330) followed at a total of 15 centers were included in the study. The mean age of the patients was 37.8 years, and 86% were women. DNA samples from the patients and healthy controls (HC; n = 210) were isolated, and the presence of HLA-B*51 or HLA-B*52 was screened for by using PCR with sequence-specific primers.We found a significant association of HLA-B*52 with TAK (20.9% vs HC = 6.7%, P = 0.000, OR = 3.7, 95% CI = 2.02 to 6.77). The distribution of HLA-B*51 did not differ between TAK patients and HCs (22.7% vs 24.8%, OR = 0.9, 95% CI = 0.60 to 1.34). The presence of HLA-B*52 decreased in late-onset patients (> 40 years of age; 12.0%, P = 0.024, OR = 0.43, 95% CI = 0.20 to 0.91). Patients with angiographic type I disease with limited aortic involvement also had a lower presence of HLA-B*52 compared to those with all other disease subtypes (13.1% vs 26%, P = 0.005, OR = 0.43, 95% CI = 0.23 to 0.78).In this study, the previously reported association of TAK with HLA-B*52 in other populations was confirmed in patients from Turkey. The functional relevance of HLA-B*52 in TAK pathogenesis needs to be explored further.Takayasu's arteritis (TAK), also known as "pulseless disease," is a chronic granulomatous panarteritis characterized by the involvement of large vessels, especially the aorta and its major branches [1,2]. Although the etiology of TAK is still unknown, infectious agents, genetic factors and autoimmunity are thought to play a major role in its pathogenesis [3]. Cell-mediated autoimmunity has been implicated in the physiopathology of vascular cell injury in TAK. In addition to ¦Ã¦Ä T cells, natural killer (NK) cells and macrophages, tissue specimens from the aortas of TAK patients are infiltrated with T cells that have a restricted T-cell repertoire, which is typical of antigen-induced proliferation [4-6].Evidences of genetic susceptibility to TAK have previously been demonstrated for SNPs of cytokine genes such as IL-2, IL-6 and IL-12 and the
%U http://arthritis-research.com/content/14/1/R27