CAJ | 학술논문

目的探讨强直性脊柱炎(AS)患者外周血T细胞受体β链可变区互补决定区3(TCRBV CDR3)谱系多态性,为AS免疫发病机制研究提供实验依据.方法采用反转录-聚合酶链反应(RT-PCR)扩增AS患者外周血单个核细胞(PBMC)中T细胞TCR BV的26个亚家族CDR3,经免疫扫描谱型技术分析TCR BV CDR,3的谱系多态性情况.结果 20例活动期AS患者TCR BV CDR3扫描谱型均出现非正态的异常峰型,包括单峰、寡峰/寡峰趋势、偏峰和不规则异常峰型.其中有18例患者部分亚家族出现寡克隆/寡克隆趋势增生,有1例患者BV16和BV18的2个亚家族出现单克隆增生.5名健康对照PBMC TCR BV CDR3谱型绝大多数呈高斯分布.结论 AS患者外周血TCR BV CDR3谱系具有显著多态性和谱系漂移特点,进一步表明T细胞在AS免疫发病机制中扮演重要角色.单/寡克隆增生的T细胞有可能是AS发病中的自身反应性T细胞.
목적 탐토강직성척주염(AS)환자외주혈T세포수체β련가변구호보결정구3(TCRBV CDR3)보계다태성,위AS면역발병궤제연구제공실험의거.방법 채용반전록-취합매련반응(RT-PCR)확증AS환자외주혈단개핵세포(PBMC)중T세포TCR BV적26개아가족CDR3,경면역소묘보형기술분석TCR BV CDR,3적보계다태성정황.결과 20례활동기AS환자TCR BV CDR3소묘보형균출현비정태적이상봉형,포괄단봉、과봉/과봉추세、편봉화불규칙이상봉형.기중유18례환자부분아가족출현과극륭/과극륭추세증생,유1례환자BV16화BV18적2개아가족출현단극륭증생.5명건강대조PBMC TCR BV CDR3보형절대다수정고사분포.결론 AS환자외주혈TCR BV CDR3보계구유현저다태성화보계표이특점,진일보표명T세포재AS면역발병궤제중분연중요각색.단/과극륭증생적T세포유가능시AS발병중적자신반응성T세포.
Objective To study the T cells lineage polymorphism of TCR BV CDR3 in the peripheral blood of ankylosing spondylitis (AS) patients,in order to provide experimental basis for the immunological patho-genesis study of AS.Methods Twenty-six subfamilies of CDR3 T cells of TCR BV in the PBMC of AS patients were amplified by RT-PCR method,then TCR BV CDR3 lineages polymorphism were analyzed by immunization scanning spectrum.Results TCR BV CDR3 scanning spectrum of 20 active AS patients showed abnormal distribution peak,including monoclonal,oligoclonal/oligoclonal trend,skewing peak and irregular abnormal peak.Among them,some subfamilies of 18 patients showed oligoclonal/oligoclonal trend expansion,BV16 and BV18 two subfamilies of one case showed monoclonal expansion.Most spectral type of PBMC TCR BV CDR3 in five normal controls showed Gauss distribution.Conclusion TCR BV CDR3 lineage have significant characteristic polymorphism and spectrum drift characteristics in the peripheral blood of AS patients,which further indicate that T cells has plaied an important role in the immunological pathogenesis of AS.Monoclonal/oligoclonal expansion of T cells may be autoreactive T cells in nature and they may be involved in the pathogenesis of AS.