EBioMedicine · 2019
TCR repertoire and CDR3 motif analyses depict the role of αβ T cells in Ankylosing spondylitis.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Zheng Ming, Zhang Xin, Zhou Yinghui, Tang Juan, Han Qing, Zhang Yang, Ni Qingshan, Chen Gang, Jia Qingzhu, Yu Haili, Liu Siqi, Robins Elizabeth, Jiang Ning Jenny, Wan Ying, Li Qi-Jing, Chen Zhi-Nan, Zhu Ping
Аннотация
BACKGROUND: Ankylosing spondylitis (AS) is a chronic inflammatory disease with worldwide high prevalence. Although AS is strongly associated with HLA-B27 MHC-I antigen presentation, the role played by αβ T cells in AS remains elusive.
METHODS: Utilizing TCRβ repertoire sequencing and bioinformatics tools developed in house, we analyzed overall TCR repertoire structures and antigen-recognizing CDR3 motifs in AS patients with different disease activities.
FINDINGS: We found that disease progression is associated with both CD4+ and CD8+ T cell oligo-clonal expansion, which suggests that αβ T cell activation may mediate AS disease progression. By developing a bioinformatics platform to dissect antigen-specific responses, we discovered a cell population consisting of both CD4+ and CD8+ T cells expressing identical TCRs, herein termed CD4/8 T cells. CD4/8 clonotypes were highly enriched in the spondyloarthritic joint fluid of patients, and their expansion correlated with the activity of disease.
INTERPRETATION: These results provide evidence on the T cell clone side to reveal the potential role of CD4/8 T cells in the etiology of AS development.
METHODS: Utilizing TCRβ repertoire sequencing and bioinformatics tools developed in house, we analyzed overall TCR repertoire structures and antigen-recognizing CDR3 motifs in AS patients with different disease activities.
FINDINGS: We found that disease progression is associated with both CD4+ and CD8+ T cell oligo-clonal expansion, which suggests that αβ T cell activation may mediate AS disease progression. By developing a bioinformatics platform to dissect antigen-specific responses, we discovered a cell population consisting of both CD4+ and CD8+ T cells expressing identical TCRs, herein termed CD4/8 T cells. CD4/8 clonotypes were highly enriched in the spondyloarthritic joint fluid of patients, and their expansion correlated with the activity of disease.
INTERPRETATION: These results provide evidence on the T cell clone side to reveal the potential role of CD4/8 T cells in the etiology of AS development.