Nishimura Wester Eidi, Sachetto Zoraida, Costallat Lilian Teresa Lavras, Yazbek Michel Alexandre, Londe Ana Carolina Santos, Guariento Edilaine Gildo, Marques Silvia Barbosa Dutra, Bertolo Manoel Barros
Department of Rheumatology, University of Campinas (UNICAMP), Campinas, SP, Brazil.
Department of Hematology, University of Campinas (UNICAMP), Campinas/, SP, Brazil.
Clinics (Sao Paulo). 2015 Jun;70(6):408-12. doi: 10.6061/clinics/2015(06)04. Epub 2015 Jun 1.
Rheumatoid arthritis is a polygenically controlled systemic autoimmune disease. Rheumatoid vasculitis is an important extra-articular phenotype of rheumatoid arthritis that can result in deep cutaneous ulcers. The objective of this study was to establish a correlation between the frequency of major histocompatibility complex class I/II alleles and killer immunoglobulin-like receptor genotypes in patients with cutaneous rheumatoid vasculitis.
Using the Scott & Bacon 1984 criteria to diagnose rheumatoid vasculitis and after excluding any other causes such as diabetes, atherosclerosis, adverse drug reactions, infection, and smoking, patients who met the criteria were selected. All of the selected rheumatoid vasculitis patients presented deep cutaneous ulcers. Identification of the major histocompatibility complex class I/II and killer immunoglobulin-like receptor genotypes was performed by polymerase chain reaction assays of samples collected from the 23 rheumatoid vasculitis patients as well as from 80 controls (40 non-rheumatoid vasculitis RA control patients and 40 healthy volunteers).
An association between the presence of the HLA-DRB11402 and HLA-DRB10101 alleles and cutaneous lesions in rheumatoid vasculitis patients and a correlation between the inhibitor KIR2DL3 and the HLA-C*0802 ligand in rheumatoid vasculitis patients were found.
An association was found between the presence of the HLA-DRB11402 and HLA-DRB10101 alleles and the development of cutaneous lesions in rheumatoid vasculitis patients. Additionally, the HLA-C*0802 ligand protects these individuals from developing cutaneous lesions.
类风湿关节炎是一种多基因控制的全身性自身免疫性疾病。类风湿血管炎是类风湿关节炎一种重要的关节外表现型,可导致深部皮肤溃疡。本研究的目的是建立皮肤型类风湿血管炎患者主要组织相容性复合体I/II类等位基因频率与杀伤细胞免疫球蛋白样受体基因型之间的相关性。
采用Scott&Bacon 1984标准诊断类风湿血管炎,排除糖尿病、动脉粥样硬化、药物不良反应、感染和吸烟等任何其他病因后,选取符合标准的患者。所有入选的类风湿血管炎患者均出现深部皮肤溃疡。通过聚合酶链反应分析从23例类风湿血管炎患者以及80例对照(40例非类风湿血管炎类风湿关节炎对照患者和40例健康志愿者)采集的样本,鉴定主要组织相容性复合体I/II类和杀伤细胞免疫球蛋白样受体基因型。
发现HLA-DRB11402和HLA-DRB10101等位基因的存在与类风湿血管炎患者的皮肤病变之间存在关联,以及抑制剂KIR2DL3与类风湿血管炎患者的HLA-C*0802配体之间存在相关性。
发现HLA-DRB11402和HLA-DRB10101等位基因的存在与类风湿血管炎患者皮肤病变的发生之间存在关联。此外,HLA-C*0802配体可保护这些个体不发生皮肤病变。