Induction of murine spiral artery modification by recombinant human interferon-gamma
Induction of murine spiral artery modification by recombinant human interferon-gamma
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DOI：
10.1016/j.placenta.2004.10.016
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发表时间：
2005-11-01
期刊：
影响因子：
3.8
通讯作者：
Croy, BA
中科院分区：
文献类型：
--
作者：
Monk, JM;Leonard, S;Croy, BA
在小鼠妊娠期间，子宫自然杀伤（uNK）细胞的功能是维持基底蜕膜和促进子宫螺旋动脉修饰，这一过程导致薄壁、扩张、细长的动脉具有降低的阻力。小鼠模型表明螺旋动脉修饰是由uNK细胞释放细胞因子干扰素（IFN）-γ引发的。本研究的目的是确定人IFN-γ是否可以诱导妊娠淋巴样（uNK-、NK-、T-、B-）小鼠中未修饰螺旋动脉的结构变化。通过每日注射rhIFN-γ，以剂量反应方式修饰妊娠Rag 2缺失/共同细胞因子链（c）γ缺失小鼠的螺旋动脉。给予低剂量LPS不会引起形态学上公认的结构变化。这些发现在构建人源化鼠妊娠模型中是关键的，因为它们表明Rag 2缺失/γ c缺失小鼠提供了在体内条件下检测人uNK细胞功能的生物测定系统。
Functions of uterine natural killer (uNK) cells during mouse pregnancy are maintenance of decidua basalis and promotion of uterine spiral artery modification, a process that results in thin-walled, dilated, elongated arteries with lowered resistance. Murine models indicate spiral artery modifications are triggered by release of the cytokine interferon (IFN)-gamma from uNK cells. The purpose of this study was to determine if human IFN-gamma could induce structural changes in the unmodified spiral arteries found in pregnant, alymphoid (uNK-, NK-, T-, B-) mice. Spiral arteries in pregnant Rag2 null/common cytokine chain (c) gamma null mice were modified, in a dose response manner, by daily injections of rhIFN-gamma. Administration of low dose LPS did not induce morphologically recognized structural changes. These findings are key in building humanized murine models of pregnancy since they suggest Rag2 null/gamma c null mice provide a bioassay system that would detect the functioning of human uNK cells under in vivo conditions.