Plasma interleukin-22 level, variants in interleukin-22 gene polymorphism, and the severity of systemic lupus erythematosus among Egyptian pediatric and adolescents

Abstract

Objectives Our purpose was to investigate, for the first time, genotypes and alleles distribution of two single nucleotide polymorphisms (SNPs) of interleukin 22 (IL-22) (rs1012356 and rs2227485) in Egyptian pediatric and adolescents with systemic lupus erythematosus (SLE) and to evaluate the plasma IL-22 levels and their association with gene polymorphism and SLE risk and severity. Methods The TaqMan™ SNP genotyping assay on a real-time polymerase chain reaction (PCR) system was employed to evaluate the polymorphism’s genotypes. Plasma IL-22 levels were determined by using an enzyme-linked immunoabsorbent assay (ELISA). Results The frequencies and genotypes of rs2227485 and rs1012356 in IL-22 between SLE patients and controls also haplotypes formed by the same SNPs revealed no statistically significant difference ( p > 0.05). Otherwise, logistic regression analysis revealed that patients carrying rs1012356 “TA + AA” genotype had increased risk for prediction of SLE activity (OR = 1.610, 95% CI = 1.339–2.760, p = 0.034) by lowering plasma IL-22 level. Conclusions Among Egyptian pediatric and adolescents, we confirm a combined model “TA + AA” in rs1012356 (A/T) of IL-22 in regression analysis, as an independent predictor for SLE activity by lowering IL-22 plasma levels. Despite neither SNP rs2227485 A/G in IL-22 gene nor haplotypes formed by the same two SNPs (rs2227485 A/G and rs1012356 A/T) were significantly associated with the clinical and/or laboratory manifestations of SLE.

Association of STAT3 gene polymorphisms with systemic lupus erythematosus in a Chinese Han population

“…2 To date, numerous studies have investigated single nucleotide polymorphisms (SNP) of genes in SLE risk, such as growth differentiation factor 15 (GDF-15), cytotoxict-lymphocyte-associated protein (CTLA), and interleukin-22 (IL-22). [3][4][5] However, discovery of more genetic polymorphisms in SLE will better elucidate pathogenesis of the disease.…”

Association of the Gelatinase B/Metalloproteinase 9 (MMP-9) Gene Haplotype in Systemic Lupus Erythematosus (SLE) in the Pediatric Egyptian Population

“…For example, it contributes to nephropathies [ 1 ], severe renal failure [ 2 , 3 ], liver cell dysfunction [ 4 ], and systemic lupus erythematosus (SLE) disease [ 5 , 6 ]. The latter is marked by permanent systemic inflammation and implicates several organs [ 5 , 6 , 7 ]; it reveals numerous clinical manifestations, together with immune complex sedimentations in kidneys and other organs. It is characterized by the formation of a wide range of autoantibodies versus various antigens (nuclear, cytoplasmic, and cell surface), and various deteriorations of the functioning of B-lymphocyte and T-cell [ 8 ].…”