Elevated levels of dehydroepiandrosterone as a potential mechanism of dendritic cell impairment during pregnancy.
Elevated levels of dehydroepiandrosterone as a potential mechanism of dendritic cell impairment during pregnancy.
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DOI：
10.1186/s12865-014-0065-9
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发表时间：
2015-01-31
期刊：
影响因子：
3
通讯作者：
Pasman NM
中科院分区：
文献类型：
--
作者：
Chernykh ER;Leplina OY;Tikhonova MA;Seledtsova NV;Tyrinova TV;Khonina NA;Ostanin AA;Pasman NM
本研究的目的是验证这一假设，即免疫功能障碍和自发性流产的风险增加，在妊娠妇女高雄激素血症（HA）是由减少的树突状细胞（DCs）的耐受性潜力，导致硫酸脱氢表雄酮（DHEAS）水平升高。研究了从非妊娠妇女、正常妊娠妇女或患有HA的妊娠妇女的血液单核细胞产生的单核细胞衍生的DC的表型和功能特性，以及DHEAS对健康妊娠妇女中DC的体外作用。在正常妊娠中，DCs显示为不成熟的，其特征在于CD 83+和CD 25 + DCs的数量减少，刺激2型T细胞应答和诱导T细胞凋亡的能力降低。相比之下，来自患有HA的孕妇的DC具有成熟的表型，能够刺激1型（IFN-γ）和2型（IL-4）T细胞应答，并且特征在于较低的B7-H1表达和对CD 8 + T细胞的细胞毒活性。在健康孕妇的DCs培养物中加入DHEAS可诱导DCs成熟并增加其激活1型T细胞应答的能力。我们的数据表明，HA孕妇的DCs致耐受性潜力降低，并揭示了DHEAS介导的DCs激素调节的新机制。
This study aimed to test the hypothesis that immune dysfunction and the increased risk of spontaneous abortion in pregnant women with hyperandrogenia (HA) are caused by the reduced tolerogenic potential of dendritic cells (DCs) that results from elevated levels of dehydroepiandrosterone sulfate (DHEAS). The phenotypic and functional properties of monocyte-derived DCs generated from blood monocytes from non-pregnant women, women with a normal pregnancy, or pregnant women with HA, as well as the in vitro effects of DHEAS on DCs in healthy pregnant women were investigated. In a normal pregnancy, DCs were shown to be immature and are characterized by a reduced number of CD83+ and CD25+ DCs, the ability to stimulate type 2 T cell responses and to induce T cell apoptosis. By contrast, DCs from pregnant women with HA had a mature phenotype, were able to stimulate both type 1 (IFN-γ) and type 2 (IL-4) T cell responses, and were characterized by lower B7-H1 expression and cytotoxic activity against CD8+ T cells. The addition of DHEAS to cultures of DCs from healthy pregnant women induced the maturation of DCs and increased their ability to activate type 1 T cell responses. Our data demonstrated the reduction in the tolerogenic potential of DCs from pregnant women with HA, and revealed new mechanisms involved in the hormonal regulation of DCs mediated by DHEAS.
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