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Title: The association of interleukin-31 polymorphisms with interleukin-31 serum levels and risk of systemic lupus erythematosus. Author: Huang HT, Chen JM, Guo J, Lan Y, Wei YS. Journal: Rheumatol Int; 2016 Jun; 36(6):799-805. PubMed ID: 26769434. Abstract: Interleukin-31 (IL-31) is the most recently discovered member of the gp130/IL-6 cytokine family which is produced mainly by activated Th2 cells. IL-31 was proved to play a crucial role in autoimmune and inflammatory diseases such as atopic dermatitis, asthma, cutaneous T cell lymphomas, Kawasaki disease and allergic rhinitis. Previous studies have identified that IL-31 could significantly induce the release of proinflammatory cytokines IL-6. Moreover, a large number of studies have shown that IL-6 plays an important role in the pathogenesis of systemic lupus erythematosus (SLE). However, up to date, no study to data was reported on the relationship between IL-31 and SLE. Therefore, in the present study, we investigated the association between IL-31 polymorphisms and its serum levels with the risk of SLE in a Chinese population. We analyzed two single nucleotide polymorphisms of IL-31 gene rs7977932 C/G and rs4758680 G/T in 190 patients with SLE and 250 age- and sex-matched controls, using polymerase chain reaction-single base extension and DNA sequencing methods. Soluble IL-31 (sIL-31) levels were measured by ELISA. From this study, we found that there were significant differences in the genotype and allele frequencies of IL-31 gene rs7977932 C/G polymorphism between the group of patients with SLE and the control group (P < 0.05). sIL-31 levels were increased in patients with SLE compared with controls (P < 0.01). Moreover, genotypes carrying the IL-31 rs7977932 G variant allele were associated with increased IL-31 levels compared to the homozygous wild-type genotype in patients with SLE. The rs7977932 C/G polymorphism of IL-31 gene and its sIL-31 levels were associated with SLE in the Chinese population. Our data suggest that IL-31 gene may play a role in the development of SLE.[Abstract] [Full Text] [Related] [New Search]