Abstract
This study was carried out to determine the effects of interleukin (IL)-10 gene polymorphism 1082A/G on clinical diversity and activity of systemic lupus erythematosus (SLE), as it was shown to be associated with E26 transcription factor binding site, and to assess IL-10 concentration in SLE patients. Blood was drawn from 54 SLE patients and 27 healthy controls for DNA extraction. The single nucleotide polymorphism was identified using the PCR-restriction fragment length polymorphism, and serum sample was collected to assay IL-10 concentration. There was an increase in IL-10 concentration in SLE total patients (mean 49.5 pg/ml). Mutant allele A (76.9%) was found more frequently in SLE patients compared with allele G (23.1%). Genotype AA (66.7%) was found more frequently, followed by AG (20.4%) and GG (12.9%). IL-10 concentration was elevated in SLE patients and was shown to be associated with disease activity. IL-10 gene polymorphism is not a strong indicator to show susceptibility of the disease.
Highlights
IntroductionSystemic lupus erythematosus (SLE) is the prototypical autoimmune disease that is characterized by autoantibody production, complement activation, and immune complex deposition, leading to diverse clinical manifestations and target tissue damage [1].SLE can vary widely in its severity, both at onset and during its course; some patients may have very mild disease with mild symptoms and no serious organ involvement, whereas others may be very ill with a number of organs affected [2].Cytokines have been suggested to be involved in the pathogenesis of SLE, as they are fundamental components in the regulation of immune response, intervening in both cellular and humoral responses [3].of SLE [6,7] and the clinical improvements in SLE patients resulting from administration of anti-IL-10 monoclonal antibody support a central role for IL-10 in the pathogenesis of SLE [8].The human IL-10 gene located on lq is a susceptible region for SLE [9]
Patients were divided on the basis of the Systemic Lupus Erythematosus Disease Activity Index (SLEDAI) score into two groups: Systemic lupus erythematosus (SLE) group I, which included 27 patients whose SLEDAI score was less than 12, and SLE group II, which included 27 patients whose SLEDAI score was 12 or greater [13]
Mutant allele A was found more frequently in SLE patients compared with allele G
Summary
Systemic lupus erythematosus (SLE) is the prototypical autoimmune disease that is characterized by autoantibody production, complement activation, and immune complex deposition, leading to diverse clinical manifestations and target tissue damage [1].SLE can vary widely in its severity, both at onset and during its course; some patients may have very mild disease with mild symptoms and no serious organ involvement, whereas others may be very ill with a number of organs affected [2].Cytokines have been suggested to be involved in the pathogenesis of SLE, as they are fundamental components in the regulation of immune response, intervening in both cellular and humoral responses [3].of SLE [6,7] and the clinical improvements in SLE patients resulting from administration of anti-IL-10 monoclonal antibody support a central role for IL-10 in the pathogenesis of SLE [8].The human IL-10 gene located on lq is a susceptible region for SLE [9]. Systemic lupus erythematosus (SLE) is the prototypical autoimmune disease that is characterized by autoantibody production, complement activation, and immune complex deposition, leading to diverse clinical manifestations and target tissue damage [1]. SLE can vary widely in its severity, both at onset and during its course; some patients may have very mild disease with mild symptoms and no serious organ involvement, whereas others may be very ill with a number of organs affected [2]. Cytokines have been suggested to be involved in the pathogenesis of SLE, as they are fundamental components in the regulation of immune response, intervening in both cellular and humoral responses [3]. The human IL-10 gene located on lq is a susceptible region for SLE [9]. Three single nucleotide polymorphisms (SNPs) at 1082A/G, 819T/C, and 592A/C in the promoter region have been demonstrated [10]
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