Tourette综合征患者血清可溶性白细胞介素6受体与自身抗体表达水平的研究

Soluble interleukin-6 receptor and autoantibodies in serum of children Tourette＇ s syndrome

目的通过研究Tourette综合征（TS）患者血清自身抗体和可溶性白细胞介素6受体表达水平改变及其之间的相关性，探讨白细胞介素6受体介导的免疫调节在疾病发生中的作用。方法应用抗脑抗体（ABAb）、抗核抗体（ANA）、可溶性白细胞介素-6受体（sIL-6R）及可溶性细胞因子受体gp130（sgp130）的酶联免疫吸附法商品试剂盒，检测67例TS患者（TS组）和64名正常人（对照组）血清sIL-6R、sgp130及相应抗体的浓度，同时采用胶乳增强免疫比浊法检测抗链球菌溶血素O（ASO）水平。结果TS组血清sIL-6R（44±16）pg／L，sgp130（69±25）pg／L，均显著高于对照组[（30±9）pg／L，（47±14）pg／L]；差异均有统计学意义（P=0．000，P=0．000，P均〈0．01）。TS组血清ABAb检出率为（67％）、ANA为（53％），均显著高于对照组（3％，25％），差异均有统计学意义（P=0．000，P〈0．01；p=0．001，P〈0．01）；且ASO增高的比例（20％）高于对照组（0％）（P=0．000，P〈0．01）。TS组ABAb浓度与sgp130呈负相关（r=-0．375，P〈0．05）。结论TS患者IL-6受体和自身抗体表达异常，中枢神经组织的自身免疫损伤可能参与了疾病发生发展的病理生理过程。

Objective The purpose of our study was to investigate the presence of autoantibodies and soluble IL-6 receptor in patients with Tourtte＇s syndrome, explore the mechanism underlying the immunologic regnlation with IL-6 receptor. Methods The serum contents of anti-brain antibody（ ABAb ） , antinuelear antibody（ ANAb）, soluble IL-6 receptor （sIL-6R）, and soluble gpl30 （sgpl30） in 67 patients and 64 health indivadual were analyzed with commercialized ELISA kits, and examined the titer of antistreptolysin O in TS and control with latex enhanced immunoturbidimetry. Results The levels of sIL-6R and sgpl30 were significantly elevated in TS compared with control group （44 ± 16） pg/L NS. （30 ± 9） pg/L, P=0.000, P〈0.01 ;（69 ± 25） pg/L NS. （47 - 14） pg/L, P = 0. 000, P 〈 0. 01, respectively. The detection rate of anti-brain antibody, antinuelear antibody in TS were more than that in control group （67% NS. 3%, P=0.000P〈0.01; 53% NS. 25%, P=0. 001, P〈0.01）. Increases ASOtiter （〉250kU/L） were found in a higher portion with TS （20%） compared to control （0%）. The level of ABAb was inversely correlated with sgp 130 concentration （r = - 0. 375, P 〈 0.05 ）. Conclusion The expression of IL-6 receptor and autoantibodies are abnormal in children Tourette＇s syndrome, which suggested that the central nerous tissue autoimmune-related immunologic injuries may be involved in the pathogenesis of the disease development.