Regulation of neutrophil recruitment by A20 in the fetus and in postnatal life (B01)

A20 对胎儿和产后生活中中性粒细胞募集的调节 (B01)

• 批准号: 200805178
• 金额: --
• 依托单位: Institut für Kardiovaskuläre Physiologie und Pathophysiologie
• 依托单位国家: 德国
• 项目类别: Collaborative Research Centres
• 财政年份: 2011
• 资助国家: 德国
• 起止时间: 2010-12-31 至 2022-12-31
• 项目状态: 已结题
• 来源: https://gepris.dfg.de/gepris/projekt/200805178?language=en
• 关键词: Regulation; neutrophil; recruitment; A20; fetus

Premature infants are at high risk to develop life-threatening infections shortly after birth. This has been linked to their immature and functionally limited innate immune response. We have recently identified A20, a potent negative regulator of NF-κB signaling, as putative factor restricting innate immune responses in the fetus. Using in vivo and in vitro approaches as well as different genetic mouse models, we intend to clarify the role of A20 in innate immune cell trafficking not only during mouse and human fetal life but also in the adult organism.

早产儿在出生后不久发生危及生命的感染的风险很高。这与其不成熟和功能有限的先天免疫反应有关。我们最近鉴定了A20，一种NF-κB信号传导的有效负调节因子，作为限制胎儿先天免疫应答的假定因子。使用体内和体外方法以及不同的遗传小鼠模型，我们打算阐明A20不仅在小鼠和人类胎儿生命期间，而且在成年生物体中在先天免疫细胞运输中的作用。