ArticleRevista da Associacao Medica Brasileira (1992)2026
The interleukin-1 beta 511C>T polymorphism is associated with susceptibility to juvenile idiopathic arthritis in a Turkish population.
Article in Revista da Associacao Medica Brasileira (1992), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundJuvenile idiopathic arthritis is the most common chronic rheumatic disease of childhood, with a significant genetic component. Polymorphisms in proinflammatory cytokine genes are potential contributors to disease susceptibility. The aim of this study was to investigate the association between tumor necrosis factor-alpha (TNF-α)-308G>A (rs1800629), interleukin-1 beta (IL-1β)-511C>T (rs16944), and interleukin-6 (IL-6)-174G>C (rs1800795) variants and juvenile idiopathic arthritis in a Turkish cohort.
methodsA case-control study was conducted involving 57 juvenile idiopathic arthritis patients and 50 age- and sex-matched healthy controls. Genotyping was performed using polymerase chain reaction-restriction fragment length polymorphism. Genotype and allele distributions were compared between groups, and associations with clinical parameters (erythrocyte sedimentation rate, C-reactive protein, disease subtype) were assessed.
resultsA significant association was found between the IL-1β-511C>T polymorphism and juvenile idiopathic arthritis. The CC genotype was significantly more frequent in patients compared to controls (24.6 vs. 2.0%; p=0.004), and the C allele demonstrated a trend toward association (p=0.051). In contrast, no significant differences were observed in the genotype or allele frequencies of the TNF-α-308G>A or IL-6-174G>C variants between patients and controls. Furthermore, none of the studied polymorphisms were associated with erythrocyte sedimentation rate, C-reactive protein levels, or specific disease subtypes.
conclusionThis study identifies the IL-1β-511C>T polymorphism as a significant risk factor for juvenile idiopathic arthritis in the Turkish population, underscoring the role of the IL-1 pathway in disease pathogenesis. These findings contribute to the understanding of the ethnic-specific genetic architecture of juvenile idiopathic arthritis and suggest IL-1β as a potential candidate for further functional and pharmacogenetic studies.
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