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SLE is a systemic autoimmune disease with polyclonal B cell hyperactivity, spontaneous lymphocyte proliferation, and the production of pathogenic antibodies to self-antigens. Interleukin-6 is a pleiotropic cytokine with diverse functions including B-cell growth and differentiation. IL-6 levels have been shown to be affected by single nucleotide change from G to C at position −174 in the promoter region of the IL-6 gene.Aim of the workTo find out whether single nucleotide polymorphisms in the promoter region of the IL-6 gene (−174 G/C) constitute a genetic susceptibility for SLE and its association with various disease clinical and immunological features.Patients and methodsForty-two female SLE patients and 40 healthy controls were genotyped for IL-6 gene promoter region (−174 G/C) polymorphism using PCR. SLE patients satisfied the 1982 revised criteria of the American Rheumatism Association for the classification of SLE, with a mean age of 32.4±5.5years and mean disease duration of 5.7±1.5years. The healthy controls were matched for age and sex, with a mean age of 31.7±4.9years. All subjects were recruited from the Rheumatology and Rehabilitation and Internal Medicine Departments, Kasr El Aini Hospitals. SLE clinical and laboratory features were recorded including constitutional, hematological, joint, renal, and neuropsychiatric manifestations, oral ulcers, serositis, malar rash, and photosensitivity and CBC, liver, kidney functions and serum C3 and C4 levels. Positivity for ANAs, Anti-dsDNA and Anti-Sm antibodies were determined.ResultsGenotypic and allelic distributions showed no significant differences between SLE patients and controls. The frequency of G allele was higher than C allele in both patients (83.3% vs. 16.7%) and controls (85% vs. 15%). SLE patients with GG genotype showed significantly higher frequencies and increased risk of; constitutional manifestations at disease onset (P=0.02), OR (95% CI)=6.55 (1.22–35.12), photosensitivity (P=0.03), OR (95% CI)=4.67 (1.11–19.54), hematological disorders (P=0.02), OR (95% CI)=5.5 (1.29–23.39) and positivity of ANAs and Anti-dsDNA [P=0.046, 0.03: OR (95% CI)=7 (1.1–45.44), 6.43 (1.23–33.65), respectively]. Furthermore, those patients had significantly lower mean WBCs counts when compared to SLE patients with (GC and CC) genotypes (4.54±1.31 vs. 5.98±1.04/dl, P=0.002). Twenty-five patients had lupus nephritis (LN) proved by renal biopsy but none of them had CC genotype. LN patients with GG genotype had nearly similar mean 24-h proteinuria to those with GC genotype (2.93±1.07 vs. 2.68±1.06g/24h and P=0.39). No significant difference was found in IL-6 genotype and allele distributions when patients with diffuse proliferative glomerulonephritis (class IV), which has the worst prognostic outcome, were compared to patients with non-class IV glomerulonephritis (classes II and III) [P=0.12, 0.15, respectively].ConclusionIL-6 promoter region (−174 G/C) polymorphism does not confer susceptibility to SLE but it is related to the presence of distinct clinical and immunological features. Furthermore, the increased frequency of the high-response G allele suggests that a genetically determined high IL-6 response may have a pathogenic role

Promoter region polymorphism (−174 G/C) of interleukin-6 gene and SLE; are they associated?