| Summary: | Accumulating evidence supports the implication of long non-coding RNAs (lncRNAs) in autoimmune diseases, including systemic lupus erythematosus (SLE). LncRNA variants could impact the development and/or outcome of the disease with variable diagnostic/prognostic utility in the clinic. We aimed to explore the contribution of <i>HOTAIR</i> (rs10783618), <i>LINC-ROR</i> (rs1942347), and <i>MALAT1</i> (rs3200401) variants to SLE susceptibility and/or severity in 163 SLE patients and age-/sex-matched controls using real-time TaqMan allelic discrimination PCR. <i>HOTAIR</i> rs10783618*C/C was associated with a 77% increased risk of SLE (OR = 1.77, 95%CI = 1.09–2.87, <i>p</i> = 0.020) under the recessive model. Similarly, <i>MALAT1</i> rs3200401*T/T carriers were three times more likely to develop SLE (OR = 2.89, 95%CI = 1.42–5.90) under the recessive model. While the rs3200401*T/C genotype was associated with a 49–57% decreased risk of SLE under codominant (OR = 0.51, 95%CI = 0.31–0.82, <i>p</i> < 0.001) and over-dominant (OR = 0.43, 95%CI = 0.27–0.68, <i>p</i> < 0.001) models. <i>LINC-ROR</i> rs1942347*A/A patients were more likely to have a positive family history of SLE. At the same time, <i>HOTAIR</i> rs10783618*C/C was associated with a higher frequency of arthritis (<i>p</i> = 0.001) and the presence of oral ulcers (<i>p</i> = 0.002), while patients carrying rs10783618*T/T genotype were more likely to develop hair loss (<i>p</i> < 0.001), weight loss (<i>p</i> = 0.001), and neurological symptoms (<i>p</i> = 0.003). In conclusion, the studied lncRNAs, <i>HOTAIR,</i> and <i>MALAT1</i> gene polymorphisms confer susceptibility for SLE, providing a potential theoretical basis for their clinical translation in SLE disease.
|
|---|