ArticleJournal of translational medicine2025
Spatial multi-omics profiling uncovers metabolic heterogeneity in Sjögren's syndrome and identifies PS(36:1) as a potential therapeutic target.
Article in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Silica based nanocarriers for combination immunotherapy targeting the tumor immune microenvironment.Drug delivery and translational research · 2026Review
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Authors and funding
20 authors.
Funding
Abstract
backgroundSjögren syndrome (SS) is a common autoimmune disease characterized by lymphocytic infiltration. Describing the transcriptional and metabolic features of the disease from a spatial perspective can enhance our understanding of the disease pathogenesis and treatment;
methodsWe collected eight human labial samples, including four labial gland samples from patients with SS and from four healthy controls. We integrated single-cell RNA sequencing, spatial transcriptomics, and spatial metabolomics techniques to generate SS-associated spatial gene expression maps and spatial metabolite profiles at a single-cell resolution. We also analyzed the characteristic metabolic and genetic changes of SS samples and infiltrated CD4
resultsComprehensive data from spatial multi-omics identified the cell types and distributions within the immune microenvironment of salivary glands in SS. CCL19 was significantly increased in lymphocyte infiltration, while IGHG4 was elevated in glandular area. Linoleic acid metabolism undergoes reprogramming in SS, with alterations in lecithin, linoleic acid, 13(S)-hydroxyoctadecadienoic acid and dihomo-γ-linolenate. Furthermore, PS (36:1) was found to be abnormally enriched in lymphocyte focus, which may be related to the abnormal expression of CD74 and HLA-DRA. Also, CXCL13 corresponded to areas resembling high levels of PS(36:1) in infiltrated CD4
conclusionsThe multi-omics analysis conducted in this study enhances our understanding of the key regulatory mechanisms driving the pathogenesis of SS and offers novel insights for its precision therapy. Furthermore, PS(36:1) emerged as a potential therapeutic target for future SS research and treatment.
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