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DNA methylation regulation of LGALS9 and its interaction with inflammatory cytokines in SD (A) LGALS9 locus plots reveal consistent genetic effects across SD GWAS, cis -mQTL, and cis -eQTL datasets ( p < 1 × 10−5). (B) Three-step SMR analysis demonstrated causal relationships between DNA methylation-mediated LGALS9 gene expressions and the onset of SD (P SMR multi < 0.05; HEIDI test p > 0.01, and Cochran’s Q p > 0.05). (C) Locus comparisons of LGALS9 gene expression and inflammatory cytokines <t>(CD5,</t> IL-10, and CST5) were performed via colocalization (PPH4 > 0.5). (D) ELISA validation of serum levels of LGALS9, CD5, IL-10, and CST5 in 16 patients with SD and 16 controls. Statistical analysis: SMR criteria as in . Data sources: eQTLGen and FinnGen R10. Colocalization: PPH4 > 0.5. ELISA: p = 0.0486 for LGALS9; ∗ p < 0.05, ∗∗ p < 0.01 versus controls. Boxplots show the median and IQR.
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DNA methylation regulation of LGALS9 and its interaction with inflammatory cytokines in SD (A) LGALS9 locus plots reveal consistent genetic effects across SD GWAS, cis -mQTL, and cis -eQTL datasets ( p < 1 × 10−5). (B) Three-step SMR analysis demonstrated causal relationships between DNA methylation-mediated LGALS9 gene expressions and the onset of SD (P SMR multi < 0.05; HEIDI test p > 0.01, and Cochran’s Q p > 0.05). (C) Locus comparisons of LGALS9 gene expression and inflammatory cytokines <t>(CD5,</t> IL-10, and CST5) were performed via colocalization (PPH4 > 0.5). (D) ELISA validation of serum levels of LGALS9, CD5, IL-10, and CST5 in 16 patients with SD and 16 controls. Statistical analysis: SMR criteria as in . Data sources: eQTLGen and FinnGen R10. Colocalization: PPH4 > 0.5. ELISA: p = 0.0486 for LGALS9; ∗ p < 0.05, ∗∗ p < 0.01 versus controls. Boxplots show the median and IQR.
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DNA methylation regulation of LGALS9 and its interaction with inflammatory cytokines in SD (A) LGALS9 locus plots reveal consistent genetic effects across SD GWAS, cis -mQTL, and cis -eQTL datasets ( p < 1 × 10−5). (B) Three-step SMR analysis demonstrated causal relationships between DNA methylation-mediated LGALS9 gene expressions and the onset of SD (P SMR multi < 0.05; HEIDI test p > 0.01, and Cochran’s Q p > 0.05). (C) Locus comparisons of LGALS9 gene expression and inflammatory cytokines (CD5, IL-10, and CST5) were performed via colocalization (PPH4 > 0.5). (D) ELISA validation of serum levels of LGALS9, CD5, IL-10, and CST5 in 16 patients with SD and 16 controls. Statistical analysis: SMR criteria as in . Data sources: eQTLGen and FinnGen R10. Colocalization: PPH4 > 0.5. ELISA: p = 0.0486 for LGALS9; ∗ p < 0.05, ∗∗ p < 0.01 versus controls. Boxplots show the median and IQR.

Journal: iScience

Article Title: Interferon signaling gene expression, and DNA methylation interactions in Sjögren’s disease via mendelian randomization

doi: 10.1016/j.isci.2026.114950

Figure Lengend Snippet: DNA methylation regulation of LGALS9 and its interaction with inflammatory cytokines in SD (A) LGALS9 locus plots reveal consistent genetic effects across SD GWAS, cis -mQTL, and cis -eQTL datasets ( p < 1 × 10−5). (B) Three-step SMR analysis demonstrated causal relationships between DNA methylation-mediated LGALS9 gene expressions and the onset of SD (P SMR multi < 0.05; HEIDI test p > 0.01, and Cochran’s Q p > 0.05). (C) Locus comparisons of LGALS9 gene expression and inflammatory cytokines (CD5, IL-10, and CST5) were performed via colocalization (PPH4 > 0.5). (D) ELISA validation of serum levels of LGALS9, CD5, IL-10, and CST5 in 16 patients with SD and 16 controls. Statistical analysis: SMR criteria as in . Data sources: eQTLGen and FinnGen R10. Colocalization: PPH4 > 0.5. ELISA: p = 0.0486 for LGALS9; ∗ p < 0.05, ∗∗ p < 0.01 versus controls. Boxplots show the median and IQR.

Article Snippet: Galectin-9 regulates B cell activation by increasing colocalization with the inhibitory co-receptor CD5, thereby modulating TLR4 signal transduction.

Techniques: DNA Methylation Assay, Gene Expression, Enzyme-linked Immunosorbent Assay, Biomarker Discovery