The cytokines (IFN-γ, IL-2, IL-4, IL-10, IL-17) and Treg cytokine (TGF-β1) levels in adults with immune thrombocytopenia
The cytokines (IFN-γ, IL-2, IL-4, IL-10, IL-17) and Treg cytokine (TGF-β1) levels in adults with immune thrombocytopenia
复制标题
DOI：
10.1691/ph.2014.4528
复制
发表时间：
2014-09-01
期刊：
影响因子：
1.6
通讯作者：
Wang, Fangting
中科院分区：
文献类型：
--
作者：
Ma, Liangliang;Liang, Yan;Wang, Fangting
以往的研究表明，自身免疫性疾病可能是由辅助性T细胞（Th）、细胞因子和调节性T细胞（Treg）细胞因子失衡引起的。我们检测了成人免疫性血小板减少症（ITP）患者血浆中Th 1相关细胞因子（IFN-γ、IL-2）、Th 2相关细胞因子（IL-4、IL-10）、Th 17相关细胞因子（IL-17）和Treg相关细胞因子（TGF-β 1）的浓度，并评估了其临床意义。采用酶联免疫吸附法（ELISA）检测52例ITP患者和30例年龄、性别匹配的健康对照者血浆IFN-γ、IL-2、IL-4、IL-10、IL-17和TGF-β 1水平。ITP患者外周血Th 2细胞因子IL-4、IL-10水平显著高于对照组（P < 0.05）。Th 1型细胞因子IFN-γ、IL-2、Th 17型细胞因子IL-17和Treg型细胞因子TGF-β在ITP患者中浓度较低（P < 0.05）。慢性ITP患者IL-17浓度显著高于重度ITP患者（P < 0.05），其他各亚组间细胞因子浓度差异无显著性，ITP患者IFN-γ浓度与PAIgG浓度呈显著正相关（r = 0.48，P = 0.02）。其他细胞因子水平与血小板计数之间、细胞因子水平与巨核细胞数量之间、细胞因子水平与PAIgG或GPIIb/IIIa和/或GPIb/IX自身抗体之间均未发现显著相关性。本研究表明Th和Treg细胞因子的失衡可能介导ITP的发病机制。
Previous studies have indicated that autoimmune diseases might be caused by an imbalance of T helper cells (Th), cytokines, and regulatory T cells(Treg) cytokines. We measured the plasma concentrations of Th1-associated cytokines (IFN-gamma, IL-2), Th2 -associated cytokines (IL-4, IL-10), Th17-associated cytokine (IL-17) and Treg -associated cytokine (TGF-beta 1) in adult patients with immune thrombocytopenia (ITP) and evaluated their clinical relevance. Plasma IFN-gamma, IL-2, IL-4, IL-10, IL-17 and TGF-beta 1 concentrations of 52 ITP patients and 30 age- and sex-matched healthy controls were measured by enzyme-linked immunosorbent assay method (ELISA). Concentration of Th2 cytokines (IL-4 and IL-10) were significantly higher in ITP patients compared to controls (P < 0.05). However, concentrations of Th1 cytokines IFN-gamma, IL-2), Th17 cytokine (IL-17) and Treg cytokine (TGF-beta) were lower in ITP patients (P < 0.05). Concentration of IL-17 was significantly higher in chronic ITP patients compared to severe ITP patients (P < 0.05), and no significant difference of cytokine concentration among the other subgroups in ITP patients was found. Among the ITP patients, concentration of IFN-gamma correlated positively and significantly with PAIgG (r = 0.48, P = 0.02). A significant correlation was neither found between other cytokine levels and platelet count, nor between cytokine levels and megakaryocytes number, nor between cytokines levels and PAIgG or GPIIb/IIIa and/or GPIb/IX autoantibodies. The present study demonstrates that an imbalance of Th and Treg cytokines may mediate the pathogenesis of ITP.