AI Article Synopsis
- Autotaxin is a key enzyme linked to diseases like cancer and autoimmune disorders, and this study focused on its role in systemic lupus erythematosus (SLE) using data from a large database called ImmuNexUT.
- Researchers found that serum levels of autotaxin were significantly higher in SLE patients compared to healthy controls, especially in specific immune cells known as plasmacytoid dendritic cells (pDCs).
- The study identified a correlation between autotaxin expression and disease activity, suggesting that genetic factors and interferon-related genes may influence its expression and contribute to SLE pathogenesis.
Article Abstract
Background: The importance of autotaxin, an enzyme that catalyzes lysophospholipid production, has recently been recognized in various diseases, including cancer and autoimmune diseases. Herein, we examined the role of autotaxin in systemic lupus erythematosus (SLE), utilizing data from ImmuNexUT, a comprehensive database consisting of transcriptome data and expression quantitative trait locus (eQTL) data of immune cells from patients with immune-mediated disorders.
Methods: Serum autotaxin concentrations in patients with SLE and healthy controls (HCs) were compared. The transcriptome data of patients with SLE and age- and sex-matched HCs were obtained from ImmuNexUT. The expression of , the gene encoding autotaxin, was examined in peripheral blood immune cells. Next, weighted gene correlation network analysis (WGCNA) was performed to identify genes with expression patterns similar to . The ImmuNexUT eQTL database and public epigenomic databases were used to infer the relationship between autotaxin and pathogenesis of SLE.
Results: Autotaxin levels were elevated in the serum of patients with SLE compared to HCs. Furthermore, the expression of was higher in plasmacytoid dendritic cells (pDCs) than in other immune cell subsets, and its expression was elevated in pDCs of patients with SLE compared to HCs. In WGCNA, belonged to a module that correlated with disease activity. This module was enriched in interferon-associated genes and included genes whose expression was influenced by single-nucleotide polymorphisms associated with SLE, suggesting that it is a key module connecting genetic risk factors of SLE with disease pathogenesis. Analysis utilizing the ImmuNexUT eQTL database and public epigenomic databases suggested that the increased expression of in pDCs from patients with SLE may be caused by increased expression of interferon-associated genes and increased binding of STAT3 complexes to the regulatory region of .
Conclusions: Autotaxin may play a critical role in connecting genetic risk factors of SLE to disease pathogenesis in pDCs.
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| http://dx.doi.org/10.1177/09612033221128494 | DOI Listing |
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