中文摘要：

目的初步探讨AS患者血清中IL-1家族细胞因子和IL-34水平的变化及作用。方法采用蛋白芯片技术检测6例AS患者、4名健康对照者血清中IL-1家族细胞因子的水平；采用ELISA方法检测65例AS患者和85名健康对照者血清中IL-34的水平，并分析血清IL-34水平与AS临床实验室指标的相关关系。统计学方法采用t检验，相关性分析采用Spearman相关分析。结果与健康对照组相比，As患者血清IL-1家族细胞因子中IL-1Ra[（3302±1352）pg／ml和（10778±2764）pg／ml]、IL-36Ra[（1363±194）pg／ml和（3875±996）pg／ml]水平显著下降（t值分别为5．363和4．289，均P〈0．05），IL-1α、IL-18、IL-36α、IL-37水平明显上升（t值分别为-2．532、-5．400、-5．023和-5．783，均P〈0．05）；此外，AS患者IL-34水平显著高于健康对照组[（169±153）Dg／ml和（54±31）pg／ml，t=6．722，P〈0．01]；并且患者血清IL-34水平与CRP、ESR呈正相关（t值分别为0．304和0．344，P均〈0．05）；HLA-B27阳性组的IL-34水平明显高于HLA-B27阴性组（P〈0．05）。结论IL-1家族部分成员和IL-34作为重要的细胞因子，可能参与了AS的炎症和免疫反应。

英文摘要：

Objective To preliminarily investigate the levels of intedeukin （IL）-I family and IL-34 in serum of patients with ankylosing spondylitis （AS） and their roles. Methods Serum IL-1 family levels were detected from 6 AS patients and 4 healthy controls by using protein-chip technique. Enzyme-linked immunosorbent assay （ELISA） method was used to detect the levels of serum IL-34 from 65 AS patients and 85 healthy controls and the relationships of serum IL-34 levels and clinical or laboratory features were analyzed. T test and Spearman correlation were used for statistical analysis. Results IL-1Ra [（3 302±1 352） pg/ml vs （10 778±2 764） pg/ml]and IL-36Ra [（1 363±194） pg/ml vs （3 875±996） pg/ml] levels were significantly down-regulated in AS patients compared with that of healthy controls （t=5.363 and 4.289 respectively, both P〈0.05）. The levels of IL-1α, IL-18, IL-36α and IL-37 were increased more remarkable in AS patients than in healthy controls （t=-2.532, -5.400, -5.023 and -5.783 respectively, both P〈0.05）. Moreover, serum IL-34 levels were elevated more significantly in AS patients than in healthy controls [（169±153） pg/ml vs （54±31） pg/ml, t=6.722, P〈0.01] and were positively correlated with the levels of CRP and ESR. Serum IL-34 levels were markedly up-regulated in human leukocyte antigen （HLA）-B27 positive patients than in HLA-B27 negative patients （P〈0.05）. Conclusion Part of IL-1 family and IL-34 may be involved in inflammatory or immunological process of AS.