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Glomerulonephritis is a major determinant of the course and prognosis of systemic lupus erythematosus (SLE) and is evident in 40%-85% of patients. IL10, a cytokine produced by monocytes and-to a lesser extent-lymphocytes, has pleiotropic effects in immune regulation and inflammation. It enhances B cell survival, proliferation, differentiation, and antibody production; these effects play a role in autoimmune diseases. Among identified polymorphisms in the IL10 promoter, three linked single nucleotide polymorphisms (SNPs) of -1082 G/A, 819 T/C, and -592 A/C have been shown to influence the IL10 gene expression. Compared with the -592 C allele, the 592 A is associated with lower IL10 production in vitro. The objectives of this study were to investigate the -592 A/C polymorphism in patients with and without lupus nephritis and to assess its influence on IL10 secretion in vivo and its role in pathogenesis and clinicopathological characteristics of lupus nephritis.

IL10 in Lupus Nephritis: Detection and relationship with disease activity