Liu Pin, Li Lijun, Fan Panpan, Zheng Junwen, Zhao Dongchi
Pediatrics and Neonatology Department, Zhongnan Hospital of Wuhan University, Donghu road 169, Wuhan, 430071, China.
BMC Pediatr. 2018 Feb 21;18(1):74. doi: 10.1186/s12887-018-1055-5.
Intravenous immunoglobulin (IVIG) is commonly used to improve the immunomodulatory effects, although its regulatory effect on premature Treg cells is unclear. The purpose of this study is to study the effect of high dose of IVIG (HD-IVIG) on Treg cells expression and cytokine profile in premature birth.
Fifty-two premature infants were enrolled in this study and thirty-one premature infants who were suspected to have intrauterine infection received HD-IVIG (1-2 g/kg) at the first day of birth; the remaining 21 premature infants were assigned as the control group. The peripheral blood CD4 + T and foxp3+ Treg cells were checked by flow cytometry, and cytokine concentrations were detected by cytometric bead array.
With the gestational age growth, peripheral blood CD4 + T and foxp3+ Treg cells of prematurity gradually declined from 50% to 35% and from 8% to 6%, respectively. Meanwhile, HD-IVIG increased the percentage of CD4 + T and foxp3+ Treg cells compared with their baseline levels (p < 0.001). HD-IVIG demonstrated different regulating effects on cytokines secretion, increased IL-17 and TGF-β, and inhibited IL-6 secretion.
Our results demonstrated that HD-IVIG not only enhanced the premature immune tolerance, but also suppressed the excessive inflammation response mediated by IL-6.
This study was under the clinical study registration (ChiCTR-ORC-16008872, date of registration, 2016-07-21).
静脉注射免疫球蛋白(IVIG)常用于改善免疫调节作用,但其对早产Treg细胞的调节作用尚不清楚。本研究旨在探讨高剂量IVIG(HD-IVIG)对早产中Treg细胞表达及细胞因子谱的影响。
本研究纳入52例早产儿,其中31例疑似宫内感染的早产儿在出生首日接受HD-IVIG(1-2 g/kg)治疗;其余21例早产儿作为对照组。采用流式细胞术检测外周血CD4+T和foxp3+Treg细胞,采用细胞计数珠阵列检测细胞因子浓度。
随着胎龄增长,早产儿外周血CD4+T和foxp3+Treg细胞分别从50%逐渐下降至35%,从8%逐渐下降至6%。同时,与基线水平相比,HD-IVIG增加了CD4+T和foxp3+Treg细胞的百分比(p<0.001)。HD-IVIG对细胞因子分泌表现出不同的调节作用,增加IL-17和TGF-β,抑制IL-6分泌。
我们的结果表明,HD-IVIG不仅增强了早产免疫耐受性,还抑制了IL-6介导的过度炎症反应。
本研究已在临床研究注册中心注册(ChiCTR-ORC-16008872,注册日期,2016-07-21)。