Ye Xin, Zhang Lei, Wang Hui, Chen Yan, Zhang Weiwei, Zhu Rongrong, Fang Chaoping, Deng Anmei, Qian Baohua
Department of Transfusion Medicine, Changhai Hospital, Second Military Medical University, 168 Changhai Road, Shanghai, 200433, China.
Department of Laboratory Diagnosis, Changhai Hospital, Second Military Medical University, 168 Changhai Road, Shanghai, 200433, China.
PLoS One. 2015 Jan 26;10(1):e0117704. doi: 10.1371/journal.pone.0117704. eCollection 2015.
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.
背景：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。本研究旨在探讨白细胞介素-23（IL-23）/辅助性T细胞17（Th17）通路在ITP患者中的作用。 方法：采用定量实时聚合酶链反应分析ITP患者和健康对照者中IL-17、IL-23及其受体的基因表达。采用酶联免疫吸附测定法检测血浆中IL-17和IL-23水平。采用流式细胞术检测Th17细胞频率。分析血浆IL-23与IL-17水平、Th17细胞、血小板之间的相关性。用IL-23刺激后，采用酶联免疫吸附测定法检测Th17相关细胞因子水平。随后，测定患者治疗后的IL-23和IL-17水平。 结果：ITP患者外周血单个核细胞中IL-23p19、IL-12p40、IL-23R、IL-12Rβ1、IL-17A、IL-17F和维甲酸相关孤儿受体C（RORC）的mRNA表达水平均升高。此外，这些ITP患者中还观察到Th17细胞以及血浆IL-17、IL-23水平升高。此外，发现血浆中IL-23水平与IL-17水平和Th17细胞呈正相关，但与血小板计数呈负相关。体外经IL-23刺激后IL-17水平显著升高。此外，有效治疗后IL-23和IL-17水平均降低。 结论：IL-23/Th17通路可能通过增强Th17反应参与ITP的发病机制。此外，我们的结果表明，IL-23/Th17通路是未来ITP治疗尝试中的一个潜在治疗靶点。
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