Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The etiology of systemic lupus erythematosus (SLE) involves a complex interaction of genetic and environmental factors. Investigations have shown that environmentally driven epigenetic changes contribute to the etiology of SLE. Here, we hypothesize that aberrant DNA methylation may contribute to the activation of the immune machinery and trigger lupus disease activity. A whole genome methylation array was applied to investigate the DNA methylation changes between 12 pairs of active SLE patients and healthy controls. The results were further confirmed in 66 SLE patients, 102 healthy controls. The methylation statuses of the IL10 and IL1R2 genes were significantly reduced in the SLE patient samples relative to the healthy controls (age-adjusted odds ratios, 64.2 and 16.9, respectively, P<0.0001). There was a trend toward SLE patients having hypomethylated IL10 and IL1R2 genes accompanied by greater disease activity. We observed that the methylation degree of IL10 and IL1R2 genes were reduced in the rheumatoid arthritis (RA) patients as well but the hypomethylation change was more significant in IL1R2 genes than in the IL10 genes in RA patients. This study demonstrated that DNA hypomethylation might be associated with SLE. Hypomethylated IL10 and IL1R2 genes may provide potential epigenetic markers as clinical predictors for autoimmune diseases.
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PMID:A whole genome methylation analysis of systemic lupus erythematosus: hypomethylation of the IL10 and IL1R2 promoters is associated with disease activity. 2204 55

Systemic lupus erythematosus (SLE) possesses a gender-dependent incidence characterized by a male/female ratio 1:9. B-cell, a vital part of the immune system, plays an important role in pathogenesis of SLE. Thus, we hypothesize that gender differences of B cells may exist in SLE and relate to the onset and the progression of SLE. Here, we showed that the genes expression pattern is similar between healthy female and male. However, SLE female and SLE male showed more upregulated genes, in which the trendline of SLE male is higher than that of SLE female. The most differentially expressed genes between SLE male patients and female patients are only on two chromosomes. While the differentially expressed genes between healthy male and female are distributed on several chromosomes. There are more differentially expressed genes in SLE male vs healthy male than these in SLE female vs healthy female. OAS3, RGS13, STAG3, IFI44L, STS-1, FERIL14, ZBTB16, USP18, USP41, RSAD2, FKBP5, IL1R2, DNAPTP6 and ILI27, which top 14 significantly upregulated mRNAs in SLE patients compared with healthy donors, showed different expression pattern in gender-based analyses. Furthermore, we revealed that this difference may be related to estrogen-induced IFI44L/BAFF. Therefore, we conclude that the diagnosis and treatment of these immune-related diseases should consider the baseline gender-related differences.
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PMID:Gender differences of B cell signature related to estrogen-induced IFI44L/BAFF in systemic lupus erythematosus. 2792 69