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Hereditary predisposition to low interleukin-10 production in children with extended oligoarticular juvenile idiopathic arthritis.

机译:遗传性诱因导致儿童少关节型青少年特发性关节炎的白细胞介素10生成量降低。

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摘要

OBJECTIVE: To determine whether children with extended oligoarticular juvenile idiopathic arthritis (JIA) produce less of the anti-inflammatory cytokine interleukin-10 (IL-10) than those with persistent oligoarticular JIA. METHODS: We measured IL-10 production in the parents of children with oligoarticular or extended oligoarticular JIA, from whole-blood cultures stimulated with lipopolysaccharide. RESULTS: IL-10 production was lower in the parents of children with extended oligoarticular JIA compared with those of children with oligoarticular JIA (P=0.034). There was an increase in the percentage of ATA-containing genotypes (i.e. genotypes ATA/ATA, ATA/ACC or ATA/GCC) in the parents of children with extended oligoarticular JIA compared with healthy controls (P<0.02) but not in the parents of children with oligoarticular JIA. CONCLUSIONS: As approximately 84% of the variation in IL-10 production is thought to be genetically regulated, these results suggest that stimulated IL-10 production would be lower in children with extended oligoarticular JIA. Because IL-10 is an anti-inflammatory cytokine, this may partly explain why this group of children has more severe disease.
机译:目的:确定与长期持续性少关节型JIA患儿相比,延长性少关节型青少年特发性关节炎(JIA)患儿是否产生较少的抗炎细胞因子白介素10(IL-10)。方法:我们测量了由脂多糖刺激的全血培养的少关节型或延长型少关节型JIA患儿父母的IL-10产生。结果:与小关节JIA患儿相比,小关节JIA患儿的父母IL-10产生较低(P = 0.034)。与健康对照组相比,患有少关节型JIA的儿童父母的含ATA基因型(即ATA / ATA,ATA / ACC或ATA / GCC基因型)的百分比有所增加(P <0.02),但父母没有少关节型JIA患儿。结论:由于认为IL-10产生的变异中约84%受基因调控,因此这些结果表明,患有延长性少关节型JIA的儿童的IL-10产生刺激性较低。因为IL-10是一种抗炎细胞因子,所以这可以部分解释为什么这组儿童患有更严重的疾病。

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