Characterization of peripheral blood TCR repertoire in patients with ankylosing spondylitis by high-throughput sequencing

被引:21
作者
Cui, Jin-Huan [1 ]
Jin, Ya-bin [1 ]
Lin, Kai-Rong [1 ]
Xiao, Ping [1 ]
Chen, Xiang-ping [1 ]
Pan, Ying-ming [1 ]
Lin, Wei [1 ]
Wu, Zu-chang [1 ]
Guo, Dong-mei [2 ]
Mao, Xiao-fan [1 ]
Zhang, Chu-ling [1 ]
Lian, Wen-lue [1 ]
Luo, Wei [1 ]
机构
[1] Sun Yat Sen Univ, Foshan Hosp, Clin Res Inst, Foshan 528000, Guangdong, Peoples R China
[2] Sun Yat Sen Univ, Foshan Hosp, Dept Rheumatol, Foshan 528000, Guangdong, Peoples R China
基金
中国国家自然科学基金;
关键词
Ankylosing spondylitis (AS); Clonotypes; Diversity; T cell receptor (TCR); TCR repertoire; T-CELL EXPANSIONS; REACTIVE ARTHRITIS; HLA-B27; DISEASE; AUTOIMMUNITY; DIVERSITY; LUPUS;
D O I
10.1016/j.humimm.2018.03.007
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Ankylosing spondylitis (AS) is a chronic and progressive autoimmune disease affecting the invasion of the spine, sacroiliac joints and peripheral joints. T cells play a vital role in the underlying pathogenesis of AS, which mediated autoimmune and inflammatory responses via specific recognition of autoantigen peptides presented by susceptibility HLA. Antigen-specific T cells triggered by HLA/antigen complexes will undergo a massive expansion that forming an uneven T cell repertoire. To enhance our understanding of T-cell-mediated autoimmune in AS, we applied TCR beta chains high-throughput sequencing to AS patients for in-depth TCR repertoire analysis. A significantly lower TCR repertoire diversity was observed in peripheral blood of AS patients relative to controls. And severe patients in our AS cohort have a more restricted TCR repertoire than mild patients, suggesting that the TCR repertoire diversity might be associated with the clinical severity of disease. No V, J and VJ pairs with significant biased usage were identified, which indicated that the usage frequency deviation of certain V/J/V-J genes in AS patients is little. This is a pilot study with potentially interesting observation on reduced diversity of T cells repertoire in peripheral blood of AS patients and further studies are needed.
引用
收藏
页码:485 / 490
页数:6
相关论文
共 26 条
[1]   αβ T cell receptors as predictors of health and disease [J].
Attaf, Meriem ;
Huseby, Eric ;
Sewell, Andrew K. .
CELLULAR & MOLECULAR IMMUNOLOGY, 2015, 12 (04) :391-399
[2]   New insights from murine lupus: disassociation of autoimmunity and end organ damage and the role of T cells [J].
Bagavant, H ;
Fu, SM .
CURRENT OPINION IN RHEUMATOLOGY, 2005, 17 (05) :523-528
[3]   Molecular mimicry in the MHC. Hidden clues to autoimmunity? [J].
Baum, H ;
Davies, H ;
Peakman, M .
IMMUNOLOGY TODAY, 1996, 17 (02) :64-70
[4]   Beh‡et's disease: immunological relevance with arthritis of ankylosing spondylitis [J].
Cetin, Esin Aktas ;
Cosan, Fulya ;
Kucuksezer, Umut Can ;
Bilgic, Sema ;
Cagatay, Yonca ;
Gul, Ahmet ;
Deniz, Gunnur .
RHEUMATOLOGY INTERNATIONAL, 2013, 33 (03) :733-741
[5]  
Charles A., 2001, IMMUNOBIOLOGY IMMUNE
[6]   Inverse correlation of programmed death 1 (PD-1) expression in T cells to the spinal radiologic changes in Taiwanese patients with ankylosing spondylitis [J].
Chen, Ming-Han ;
Chen, Wei-Sheng ;
Lee, Hui-Ting ;
Tsai, Chang-Youh ;
Chou, Chung-Tei .
CLINICAL RHEUMATOLOGY, 2011, 30 (09) :1181-1187
[7]   High-throughput T cell receptor sequencing reveals distinct repertoires between tumor and adjacent non-tumor tissues in HBV-associated HCC [J].
Chen, Yunqing ;
Xu, Ying ;
Zhao, Miaoxian ;
Liu, Yu ;
Gong, Mingxing ;
Xie, Cantao ;
Wu, Hongkai ;
Wang, Zhanhui .
ONCOIMMUNOLOGY, 2016, 5 (10)
[8]   The immune dysfunction in ankylosing spondylitis patients [J].
Duan, Zhongliang ;
Gui, Yuyan ;
Li, Cui ;
Lin, Jing ;
Gober, Hans-Juergen ;
Qin, Juanxiu ;
Li, Dajin ;
Wang, Ling .
BIOSCIENCE TRENDS, 2017, 11 (01) :69-76
[9]   CD4+ and CD8+ clonal T cell expansions indicate a role of antigens inankylosing spondylitis; a study in HLA-B27+ monozygotic twins [J].
Duchmann, R ;
Lambert, C ;
May, E ;
Höhler, T ;
Märker-Hermann, E .
CLINICAL AND EXPERIMENTAL IMMUNOLOGY, 2001, 123 (02) :315-322
[10]  
Dulphy N, 1999, J IMMUNOL, V162, P3830