Journal of cellular and molecular medicine · 2024
Exploring T Cell and NK Cell Involvement in Ankylosing Spondylitis Through Single-Cell Sequencing.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Chen Tianyou, Ning Shengyu, Zhu Jichong, Zhan Xinli, Zhou Chenxing, Huang Chengqian, Wu Shaofeng, Zhang Bin, Feng Sitan, Chen Jiarui, Xue Jiang, Yang Zhenwei, Liu Chong
Аннотация
To uncover the complex immune mechanisms driving inflammation in ankylosing spondylitis and lay the groundwork for identifying new therapeutic targets and innovative approaches, we conducted 10× single-cell sequencing on bone marrow cell samples collected from the vertebrae of three AS patients and three non-AS patients. Using single-cell sequencing data, we analysed the expression of differentially expressed genes (DEGs) by comparing AS patients with non-AS patients. Key genes among the related DEGs were identified through protein-protein interaction networks and hub gene screening and further validated using immunohistochemistry. We performed clustering and annotation of the single-cell sequencing data and externally validated the findings using the GSE232131 single-cell dataset. By integrating transcriptome data, we assessed the differential expression of immune cells in AS. Finally, we explored the interactions between immune cells in AS through cell communication analysis. The upregulated gene CD74 was identified as a hub gene in T cells in AS. Further research revealed the important relationship between T cells and NK cells in the fundamental processes of AS. Additionally, we found that the macrophage migration inhibitory factor signalling pathway is prominently expressed in the interactions among various cell types in AS.
Предметные рубрики MeSH
Spondylitis, AnkylosingHumansSingle-Cell AnalysisKiller Cells, NaturalT-LymphocytesTranscriptomeGene Expression ProfilingProtein Interaction MapsGene Regulatory NetworksMaleAdultAntigens, Differentiation, B-LymphocyteFemaleSignal TransductionHistocompatibility Antigens Class IIComputational BiologyGene Expression RegulationCell Communication