The role of IL-23/Th17 pathway in patients with primary immune thrombocytopenia.
The role of IL-23/Th17 pathway in patients with primary immune thrombocytopenia.
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IL-23/Th17 通路在原发性免疫性血小板减少症患者中的作用
DOI：
10.1371/journal.pone.0117704
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发表时间：
2015
期刊：
影响因子：
3.7
通讯作者：
Qian B
中科院分区：
文献类型：
--
作者：
Ye X;Zhang L;Wang H;Chen Y;Zhang W;Zhu R;Fang C;Deng A;Qian B
原发性免疫性血小板减少症（ITP）是一种病因不明的自身免疫性出血性疾病。本研究旨在探讨IL-23/Th 17通路在ITP发病中的作用。方法采用实时荧光定量PCR技术检测ITP患者和健康对照者外周血IL-17、IL-23及其受体基因表达。ELISA法检测血浆IL-17和IL-23水平。流式细胞仪检测Th 17细胞的频率。分析血浆IL-23与IL-17、Th 17细胞、血小板的相关性。用IL-23刺激后，通过ELISA测量Th 17相关细胞因子的水平。随后，在治疗后的患者中测量IL-23和IL-17水平。结果ITP患者外周血单个核细胞IL-23 p19、IL-12 p40、IL-23 R、IL-12 R β1、IL-17 A、IL-17 F和RORC的mRNA表达水平均升高。此外，ITP患者Th 17细胞及血浆IL-17、IL-23水平也明显升高。此外，还发现血浆中IL-23水平与IL-17水平和Th 17细胞呈正相关，而与血小板计数呈负相关。在体外IL-23刺激后，IL-17水平显示出显著升高。此外，有效治疗后IL-23和IL-17水平均下降。结论IL-23/Th 17通路可能通过增强Th 17应答参与ITP的发病。此外，我们的研究结果表明，IL-23/Th 17通路是一个潜在的治疗目标，在未来的尝试治疗ITP。
Background Primary immune thrombocytopenia (ITP) is an autoimmune bleeding disorder with an unclear etiology. This study aims to investigate the role of IL-23/Th17 pathway in patients with ITP. Method The gene expressions of IL-17, IL-23 and their receptors in ITP patients and healthy controls were analyzed by quantitative real-time PCR. ELISA was used to test the IL-17 and IL-23 levels in plasma. Flow cytometry was used to detect the frequency of Th17 cells. The correlation between plasma IL-23 and IL-17 levels, Th17 cells, platelets were analyzed. The level of Th17-related cytokines was measured by ELISA following stimulation with IL-23. Subsequently, the IL-23 and IL-17 levels were measured in patients post-treatment. Results The PBMCs of ITP patients showed increased mRNA expression levels in each of the following: IL-23p19, IL-12p40, IL-23R, IL-12Rβ1, IL-17A, IL-17F, and RORC. In addition, elevated Th17 cells and plasma IL-17, IL-23 levels were also observed in these ITP patients. Furthermore, it was found that IL-23 levels in plasma are positively correlated with IL-17 levels and Th17 cells, yet negatively correlated with platelet count. Following IL-23 stimulation in vitro, IL-17 levels showed significant elevation. Furthermore, both IL-23 and IL-17 levels decreased after effective treatment. Conclusion The IL-23/Th17 pathway may be involved in the pathogenesis of ITP through enhancement of the Th17 response. Moreover, our results suggest that the IL-23/Th17 pathway is a potential therapeutic target in future attempts of ITP treatment.
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