Adoptive transfer of CD4⁺CD25⁺ regulatory T cells for prevention and treatment of spontaneous abortion

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• 作者：Yongxiang Yin^a ; Xiaofeng Han^b ; ^{yinyrh2007@hotmail.com} ; Qin Shi^c ; Yiming Zhao^d ; Yang He^d
• 关键词：CD4+CD25+ regulatory T cells ; In vitro expansion ; Spontaneous abortion ; Cytokines ; Fetal resorption rate
• 刊名：European Journal of Obstetrics and Gynecology and Reproductive Biology
• 出版年：2012
• 期刊代码：92_03012115
• 类别：med
• 出版时间：April, 2012
• 卷：161
• 期：2
• 页码：177-181
• 文件大小：345 K

摘要

Objectives

The purpose of this study was to examine whether adoptive transfer with in vitro expanded CD4⁺CD25⁺ regulatory T cells (Tregs) could prevent immune response-mediated spontaneous abortion in mice.

Study design

Female CBA/J mice were mated with male Balb/c as the control with normal pregnancy or with DBA/2J mice as a model of spontaneous abortion. The CBA/J mice mated with DBA/2J were treated intravenously with freshly isolated or in vitro expanded Tregs on day 1 or 4 of pregnancy, respectively. The numbers of surviving and reabsorbed fetuses in the different groups of mice were counted on day 14 of pregnancy, and the concentrations of cytokines in individual sera and the supernatants of cultured Tregs were measured by ELISA.

Results

Adoptive transfer with freshly isolated Tregs only slightly reduced the fetal resorption rate, which was not significantly different from that of the mice without Treg treatment, regardless of treatment at early stage and implementation of pregnancy. In contrast, adoptive transfer with in vitro expanded Tregs significantly reduced the fetal resorption rates, particularly for treatment at early stage of pregnancy (P < 0.05). Furthermore, adoptive transfer with in vitro expanded Tregs at early stage of pregnancy significantly increased the levels of serum IL-10, TGF-尾1, and the ratios of IL-10 to IFN-纬.

Conclusions

Our data clearly indicated that adoptive transfer with in vitro expanded Tregs at early stage of pregnancy protected fetuses from spontaneous abortion by re-establishing immune tolerance in mice.