STAT3 and SPI1, may lead to the immune system dysregulation and heterotopic ossification in ankylosing spondylitis

BMC Immunology

Yunfeng Nie¹  Hao Li²  Haopeng Zeng²  Tuo Liang²  Xinli Zhan²  Tianyou Chen²  Jiarui Chen²  Jiang Xue²  Zhaojie Qin²  GuoYong Xu²  Zide Zhang²  Jie Jiang²  Chong Liu²  Zhen Ye² 

[1] Guangxi Medical University;Spine and Osteopathy Ward, The First Affiliated Hospital of Guangxi Medical University;

关键词: Ankylosing spondylitis;    Th1 cells;    NKT cells;    STAT3;    SPI1;    Biomarkers;   

DOI  :  10.1186/s12865-022-00476-6

来源: DOAJ

【 摘 要 】

Abstract Objective This study was aimed to identify the biomarkers for diagnosis and reveal the immune microenvironment changes in ankylosing spondylitis (AS). Methods GSE73754 was downloaded for the co-expression network construction and immune cell analyses. Flow cytometric analysis was performed to validate the results of bioinformatics analysis. Gene set enrichment analysis (GSEA) was performed to investigate the potential biological characteristic between different phenotypes. Pearson correlation analysis between the hub genes and the xCell score of immune cell types was performed. Results Signal transducer and activator of transcription 3 (STAT3) and Spi-1 proto-oncogene (SPI1) was identified as the hub genes in the datasets GSE73754. And the t-test showed that the expression level of STAT3 and SPI1 in the GSE73754 was significantly higher in AS and human leukocyte antigen (HLA)-B27(+) groups. Flow cytometric analysis showed that natural killer T cells (NKT) cells were upregulated, while Th1 cells were down-regulated in AS, which was consistent with the results obtained from bioinformatics analysis. STAT3 and SPI1 was correlated with the NKT cells and Th1 cells. Conclusion STAT3 and SPI1 may be a key cytokine receptor in disease progression in AS.

【 授权许可】

Unknown