TRAIL mRNA expression in peripheral blood mononuclear cells of Egyptian SLE patients
- PMID: 23792015
- DOI: 10.1016/j.gene.2013.05.084
TRAIL mRNA expression in peripheral blood mononuclear cells of Egyptian SLE patients
Abstract
Although the definite etiopathogenesis of systemic lupus erythematosus (SLE) remains unclear, many different mechanisms may contribute to its pathogenesis. Tumor-necrosis factor-related apoptosis-inducing ligand (TRAIL) is a member of the tumor necrosis factor (TNF) family with pro-apoptotic activity. The accumulation of apoptotic cell debris has been hypothesized to induce the autoimmune inflammation in SLE, and TRAIL may trigger this programmed cell death. We investigated TRAIL mRNA expression levels in peripheral blood mononuclear cells (PBMCs) from 60 SLE patients and 40 controls using quantitative real-time reverse transcription-polymerase chain reaction (RT-PCR), and we studied the association between the results and clinical and laboratory parameters of the patients. Expression levels of TRAIL mRNAs in SLE patients were significantly higher than in controls (p<0.001). A statistically significant association was detected between TRAIL mRNA expression and SLE activity (p=0.001).
Keywords: ANAs; Apo2L; C3; CBC; DR4; DcR1; ESR; GAPDH; IFN; NK; PBMCs; RT-PCR; Real-time reverse transcription-polymerase chain reaction; SLE; SLEDAI; Systemic lupus erythematosus; TNF; TRAIL; Tumor necrosis factor-related apoptosis-inducing ligand; Tumor-necrosis factor-related apoptosis-inducing ligand (TRAIL); antinuclear antibodies; apoptosis ligand 2; complement; complete blood count; death receptor 4; decoy receptor 1; double-stranded deoxyribonucleic acid antibodies; dsDNA; erythrocyte sedimentation rate; glyceraldehydes-3-phosphate dehydrogenase; interferon; mRNA; messenger RNA; natural killer; peripheral blood mononuclear cells; real-time reverse transcription-polymerase chain reaction; systemic lupus erythematosus; systemic lupus erythematosus disease activity index; tumor necrosis factor.
Copyright © 2013 Elsevier B.V. All rights reserved.
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