PRODUCTION OF GRANULOCYTE-MACROPHAGE COLONY-STIMULATING FACTOR BY HUMAN TROPHOBLAST CELLS AND BY DECIDUAL LARGE GRANULAR LYMPHOCYTES
PRODUCTION OF GRANULOCYTE-MACROPHAGE COLONY-STIMULATING FACTOR BY HUMAN TROPHOBLAST CELLS AND BY DECIDUAL LARGE GRANULAR LYMPHOCYTES
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DOI：
10.1093/oxfordjournals.humrep.a138769
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发表时间：
1994-09-01
影响因子：
6.1
通讯作者：
LOKE, YW
中科院分区：
文献类型：
--
作者：
JOKHI, PP;KING, A;LOKE, YW
粒细胞-巨噬细胞集落刺激因子（GMCSF）是一种经典的造血细胞因子，与胎盘的生长和发育有关。在本研究中，我们使用酶联免疫吸附测定（ELISA）和生物测定并辅以免疫细胞化学，研究了子宫蜕膜 CD56（+）NK 细胞（大颗粒淋巴细胞）的主要子宫淋巴细胞群产生 GM-CSF 的情况，以及影响这种产生的因素。我们还研究并比较了人类妊娠早期滋养层以及 JEG-3 和 JAR 绒毛膜癌细胞产生 GM-CSF 的情况。我们的数据表明，在妊娠早期的母体蜕膜中产生了大量的 GM-CSF，并且这种分泌物的重要组成部分来自蜕膜大颗粒淋巴细胞 (LGL)。 LGL 产生的 GM-CSF 是组成型的，并且明显高于新鲜分离的外周血白细胞。通过在单层蜕膜基质细胞上共培养，可以增强蜕膜 LGL 的 GM-CSF 分泌，并且还可以通过白介素-1 (IL-1) 或 IL-2 刺激以剂量依赖性方式增加。 IL-4、IL-6、肿瘤坏死因子α（TNFα）、转化生长因子β（TGFβ）、干扰素α（IFNα）和IFNγ单独对GM-CSF分泌没有影响，尽管IL-4、TGFβ和IFNα均抑制IL-2的作用。 IFNγ对IL-2诱导的GM-CSF分泌没有影响，但拮抗IL-1的作用。正常人妊娠早期滋养层也被发现产生 GM-CSF，但 JEG-3 或 JAR 绒毛膜癌细胞未见产生任何 GM-CSF。这些结果表明，来自子宫淋巴细胞和滋养层本身的 GM-CSF 可能以旁分泌和自分泌方式影响胎盘生长和发育。
Granulocyte - macrophage colony-stimulating factor (GMCSF) is a classical haematopoietic cytokine which has been implicated in placental growth and development. In this study, we investigated the production of GM-CSF in human first trimester pregnancy by the predominant uterine lymphocyte population of decidual CD56(+) NK cells (large granular lymphocytes) and the factors that influence this production using enzyme-linked immunosorbent assays (ELISAs) and bioassays, supplemented by immunocytochemistry. We have also investigated and compared production of GM-CSF by human first trimester trophoblast and by JEG-3 and JAR choriocarcinoma cells. Our data show that appreciable amounts of GM-CSF are produced in first trimester maternal decidua and that a significant component of this secretion was from decidual large granular lymphocytes (LGL). Production of GM-CSF by LGL was constitutive and considerably greater than that of freshly isolated peripheral blood leukocytes. GM-CSF secretion by decidual LGL could be enhanced by co-culture on a monolayer of decidual stromal cells, and could also be increased in a dose-dependent manner by stimulation with interleukin-l (IL-1) or IL-2. IL-4, IL-6, tumour necrosis factor alpha (TNF alpha), transforming growth factor beta (TGF beta), interferon alpha (IFN alpha) and IFN gamma individually had no effect on GM-CSF secretion, although IL-4, TGF beta and IFN alpha all inhibited the action of IL-2. IFN gamma had no effect on the IL-2-induced GM-CSF secretion, but did antagonize the action of IL-1. Normal human first trimester trophoblast was also found to produce GM-CSF, although no production whatsoever was seen by JEG-3 or JAR choriocarcinoma cells. These results suggest that GM-CSF from uterine lymphocytes, and from trophoblast itself, may influence placental growth and development in both a paracrine and an autocrine manner.