Immunology: Production of granulocyte-macrophage colony-stimulating factor by human trophoblast cells and by decidual large granular lymphocytes
Immunology: Production of granulocyte-macrophage colony-stimulating factor by human trophoblast cells and by decidual large granular lymphocytes
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免疫学：人滋养层细胞和蜕膜大颗粒淋巴细胞产生粒细胞-巨噬细胞集落刺激因子
DOI：
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发表时间：
1994
期刊：
影响因子：
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通讯作者：
Y. W. Loke
中科院分区：
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作者：
P. P. Jokhi;A. King;Y. W. Loke
粒细胞-巨噬细胞集落刺激因子（GM-CSF）是一种经典的造血细胞因子，与胎盘的生长发育密切相关。在这项研究中，我们调查了生产的GM-CSF在人类妊娠早期的主要子宫淋巴细胞群体的蜕膜CD 56 + NK细胞（大颗粒淋巴细胞）和影响这种生产的因素，使用酶联免疫吸附试验（ELISA）和生物测定，辅以免疫细胞化学。我们还研究和比较了人早孕滋养层细胞和JEG-3及绒毛膜癌细胞的GM-CSF的产生。我们的数据表明，相当数量的GM-CSF产生于孕早期母体蜕膜，这种分泌的一个重要组成部分是从蜕膜大颗粒淋巴细胞（LGL）。LGL产生的GM-CSF是组成性的，并且比新鲜分离的外周血白细胞产生的GM-CSF要多得多。蜕膜LGL分泌的GM-CSF可以通过与单层蜕膜基质细胞共培养来增强，并且也可以通过用白细胞介素-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（TNF α）、转化生长因子β（TGF β）、干扰素α（IFN α）和IFN γ单独对GM-CSF分泌无影响，尽管IL-4、TGF β和IFN α均抑制IL-2的作用。IFN γ对IL-2诱导的GM-CSF分泌无影响，但可拮抗IL-1的作用。也发现正常人早期妊娠滋养层产生GM-CSF，尽管JEG-3或绒毛膜癌细胞没有观察到任何产生。这些结果表明，GM-CSF从子宫淋巴细胞，从滋养细胞本身，可能会影响胎盘的生长和发育，在旁分泌和自分泌的方式。
: Granulocyte-macrophage colony-stimulating factor (GM-CSF) 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-1 (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.