Literature DB >> 35065610

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

Tuo Liang1, Jiarui Chen1, GuoYong Xu1, Zide Zhang1, Jiang Xue1, Haopeng Zeng1, Jie Jiang1, Tianyou Chen1, Zhaojie Qin1, Hao Li1, Zhen Ye1, Yunfeng Nie2, Xinli Zhan1, Chong Liu3.   

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.
© 2022. The Author(s).

Entities:  

Keywords:  Ankylosing spondylitis; Biomarkers; NKT cells; SPI1; STAT3; Th1 cells

Mesh:

Substances:

Year:  2022        PMID: 35065610      PMCID: PMC8783415          DOI: 10.1186/s12865-022-00476-6

Source DB:  PubMed          Journal:  BMC Immunol        ISSN: 1471-2172            Impact factor:   3.615


  45 in total

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