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Potential common mechanisms between primary Sjögren's syndrome and Hashimoto's thyroiditis: a public databases-based study.

作者信息

Lin Yanjun, Tang Shupin, Lin Yan, Wang Rihui, Xing Yifeng, Xu Zonghe, Li Yan, Fang Qingxia, Wei Wenwei, Wu Dong, Chen Jiang

机构信息

Fujian Key Laboratory of Oral Diseases, School and Hospital of Stomatology, Fujian Medical University, Fuzhou, Fujian, China.

Department of Otorhinolaryngology-Head and Neck Surgery, the First Affiliated Hospital, Fujian Medical University, Fuzhou, Fujian, China.

出版信息

Front Genet. 2025 Apr 29;16:1520332. doi: 10.3389/fgene.2025.1520332. eCollection 2025.


DOI:10.3389/fgene.2025.1520332
PMID:40364944
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12069379/
Abstract

OBJECTIVE: Primary Sjögren's syndrome (pSS) and Hashimoto thyroiditis (HT) can occur in the same patient population, but the mechanism of co-occurrence remains unknown. This study aims to explore the underlying mechanism. METHODS: We screened differentially expressed genes (DEGs) in the pSS and HT-related transcriptomic microarrays. Based on KEGG, PID, Reactome, and BioCarta enrichment analysis, pathway annotations were performed. A PPI network was developed using STRING. Betweenness, BottleNeck, MNC, Radiality EPC, and Stress topological analyses were performed to identify hub genes. Then, we used two more datasets to validate the key genes. Immune infiltration landscape of pSS and HT were profiled based on CIBERSORT, Xcell, MCPCounter, and EPIC. Correlation between T/B cells and key genes was performed. Single gene GSEA analysis was performed to further explore enriched pathways of key genes. Finally, we predicted the drugs of key genes and the cross-talk genes targeted in the protein domain. RESULTS: A total of 93 cross-talk genes were found. These genes were mainly related to the immune system. STAT1, CD8A, and PTPRC were identified as hub genes using six topological methods. STAT1 and PTPRC are considered key genes after validation. STAT1 and PTPRC were linked to CD8 Tcm and other immune cells in the pSS and HT dataset. GSEA analysis showed that STAT1 and PTPRC may play a role in pSS and HT through several pathways, including IFNγ response, IFNα response, allograft rejection, E2F targets, complement, G2M checkpoint, IL6-JAK-STAT3 signaling, KRAS signaling up, IL2-STAT5 signaling, IL6-JAK-STAT3-signaling, and inflammatory response. Guttiferone K and picoplatin may be the candidate drugs for the treatment of pSS and HT. Cross-talk genes were mainly enriched in IGc1, MHCIIα and SCY. CONCLUSION: We analysed databases and gene expression data for pSS and HT. We identified two genes (STAT1, PTPRC) as potential biomarkers of disease activity in pSS and HT. We also gained new insights into the cellular and molecular mechanisms associated with pSS and HT. Based on the key genes and cross-talk genes, we predicted potential drugs and protein domains for pSS and HT.

摘要
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f06c/12069379/83de36c2fbbe/fgene-16-1520332-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f06c/12069379/a5518211fa8f/fgene-16-1520332-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f06c/12069379/299e7700546d/fgene-16-1520332-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f06c/12069379/6caa7bad1a68/fgene-16-1520332-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f06c/12069379/0a1da5e41b1f/fgene-16-1520332-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f06c/12069379/739594000566/fgene-16-1520332-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f06c/12069379/77f7c72a4e5a/fgene-16-1520332-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f06c/12069379/397b57a75055/fgene-16-1520332-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f06c/12069379/83de36c2fbbe/fgene-16-1520332-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f06c/12069379/a5518211fa8f/fgene-16-1520332-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f06c/12069379/299e7700546d/fgene-16-1520332-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f06c/12069379/6caa7bad1a68/fgene-16-1520332-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f06c/12069379/0a1da5e41b1f/fgene-16-1520332-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f06c/12069379/739594000566/fgene-16-1520332-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f06c/12069379/77f7c72a4e5a/fgene-16-1520332-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f06c/12069379/397b57a75055/fgene-16-1520332-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f06c/12069379/83de36c2fbbe/fgene-16-1520332-g008.jpg

相似文献

[1]
Potential common mechanisms between primary Sjögren's syndrome and Hashimoto's thyroiditis: a public databases-based study.

Front Genet. 2025-4-29

[2]
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[3]
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[4]
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[5]
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[6]
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[7]
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J Assoc Physicians India. 2023-1

[8]
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J Immunol Res. 2021

[9]
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[10]
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Clin Rheumatol. 2025-4-14

本文引用的文献

[1]
KLF4 regulates trophoblast function and associates with unexplained recurrent spontaneous abortion.

J Transl Med. 2024-10-10

[2]
Immunometabolic alteration of CD4 T cells in the pathogenesis of primary Sjögren's syndrome.

Clin Exp Med. 2024-7-22

[3]
Elevated unphosphorylated STAT1 and IRF9 in T and B cells of primary sjögren's syndrome: Novel biomarkers for disease activity and subsets.

J Autoimmun. 2024-7

[4]
CD8 tissue-resident memory T cells are expanded in primary Sjögren's disease and can be therapeutically targeted by CD103 blockade.

Ann Rheum Dis. 2024-9-30

[5]
Immunolocalization patterns of histone-deacetylases in salivary glands of mice during postnatal development.

Acta Histochem. 2024-2

[6]
Epidemiology of Sjögren syndrome.

Nat Rev Rheumatol. 2024-3

[7]
Identification of key genes in salivary gland in Sjögren's syndrome complicated with Hashimoto thyroiditis: Common pathogenesis and potential diagnostic markers.

Medicine (Baltimore). 2023-9-29

[8]
Autoimmune polyendocrine syndromes associated with autoimmune rheumatic diseases.

Reumatologia. 2023

[9]
CD4 T cell memory.

Nat Immunol. 2023-6

[10]
Potential common molecular mechanisms between Sjögren syndrome and inclusion body myositis: a bioinformatic analysis and validation.

Front Immunol. 2023

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