17β-estradiol (E2) modulates cytokine and chemokine expression in human monocyte-derived dendritic cells
17β-estradiol (E2) modulates cytokine and chemokine expression in human monocyte-derived dendritic cells
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DOI：
10.1182/blood-2003-10-3380
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发表时间：
2004-09-01
期刊：
影响因子：
20.3
通讯作者：
Clark, EA
中科院分区：
文献类型：
--
作者：
Bengtsson, ÅK;Ryan, EJ;Clark, EA
雌激素对免疫系统的影响在很大程度上仍然是未知的。我们研究了17 β-雌二醇（E-2）对人单核细胞来源的未成熟树突状细胞（IDCs）的影响。在E-2中的短期培养对iDC存活或细胞表面标志物的表达没有影响。然而，E-2处理显著增加iDC中白细胞介素6（IL-6）的分泌，并且还增加DC的骨保护素（OPG）的分泌。此外，E-2显著增加iDC分泌炎性趋化因子IL-8和单核细胞趋化蛋白1（MCP-1），但不增加组成型趋化因子胸腺和活化调节趋化因子（TARC）和巨噬细胞衍生趋化因子（MDC）的产生。然而，E-2预处理后，脂多糖（LPS）诱导的MCP-1，TARC和MDC的DC的生产明显增强。此外，成熟DC预处理E-2刺激T细胞比对照细胞。最后，我们发现E-2为成熟DC向CCL 19/巨噬细胞炎性蛋白3 β（MIP 3 β）迁移提供了必要的信号。总之，E-2可能影响DC对T细胞和B细胞反应的调节，以及帮助维持炎症反应。这可以部分解释血清雌激素水平与某些自身免疫性疾病严重程度相关的原因。(C)2004年，美国血液学会。
The effects of estrogen on the immune system are still largely unknown. We have investigated the effect of 17beta-estradiol (E-2) on human monocyte-derived immature dendritic cells (IDCs). Short-term culture in E-2 had no effect on iDC survival or the expression of cell surface markers. However, E-2 treatment significantly increased the secretion of interleukin 6 (IL-6) in iDCs and also increased secretion of osteoprotegerin (OPG) by DCs. Furthermore, E-2 significantly increased secretion of the inflammatory chemokines IL-8 and monocyte chemoattractant protein 1 (MCP-1) by iDCs, but not the production of the constitutive chemokines thymus and activation-regulated chemokine (TARC) and macrophage-derived chemokine (MDC). However, after E-2 pretreatment the lipopolysaccharide (LPS)-induced production of MCP-1, TARC, and MDC by DCs was clearly enhanced. Moreover, mature DCs pretreated with E-2 stimulated T cells better than control cells. Finally, we found that E-2 provides an essential signal for migration of mature DCs toward CCL19/macrophage inflammatory protein 3beta (MIP3beta). In summary, E-2 may affect DC regulation of T-cell and B-cell responses, as well as help to sustain inflammatory responses. This may explain, in part, the reason serum levels of estrogen correlate with the severity of certain autoimmune diseases. (C) 2004 by The American Society of Hematology.