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Background
Autoimmune diseases are defined by a shortage of adaptation to self-antigenic substances and an accompanying immune attack on tissues, cells, and organs. When the immune system attacks its tissues, damage to organs and systemic inflammation result from a systemic autoimmune illness called systemic lupus erythematosus (SLE). Certain studies have shown how miRNAs and certain SNPs are implicated in the pathogenesis of autoimmune diseases by changing the healthy immune responses [1].
The noncoding RNA clusters known as micro-RNAs, or miRNAs, range in length from 18 to 25 nucleotides. Translation and transcription are regulated by miRNAs [2]. They link to the 3′ end of the untranslated regions of the targeted mRNAs, changing translation and mRNA stability [3].
miRNAs control several biological processes in the cells, such as apoptosis, metabolism, differentiation, and development [2]. Furthermore, it has been shown that miRNAs are essential for regulating both innate and adaptive immune responses [4]. There has been conflicting evidence linking the single-nucleotide polymorphism (SNP) of miRNA 146 A (miR-146a) and miRNA 499 (miR-499) to autoimmune disorders and the release of inflammatory cytokines [5, 6].
The miR-146a gene precursor stem region at human chromosomal location 5q33.3 is home to the miR-146a (rs2910164 G > C) polymorphism locus, which causes a change in the stem structure from the G/U pair to the C/U mismatch [7]. The human chromosomal location 20q11.22 contains the miR-499 (rs374644 T/C) polymorphism, which causes a shift in the stem structure from the A/U pair to the G/U mismatch [8].
MiR-499 (rs37464444 T/C) and miR-146a (rs2910164 G > C) have been associated with several autoimmune disorders [9], including SLE [10], rheumatoid arthritis [11, 12], ankylosing spondylitis [13], and Graves’ disease [14], and have been evaluated; yet, the results are somewhat debatable. A relationship between the rs3746444 genotypes and the likelihood of developing autoimmune illnesses, such as SLE, was shown in meta-analysis research [6].
A correlation between SLE and the miR-146a and miR-499 polymorphisms has shown contradictory reports [15, 16, 17, 18, 19, 20, 21, 22–23]. For this controversy, this study aimed to determine if both SNPs of miR-499 (rs3746444 T/C) and miR-146a (rs2910164 C/G) were associated with an increased risk of developing SLE and disease activity in Egyptian patients.
Patients and methods
Ethical consideration
Patients with SLE were the subjects...
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