白介素33信号调控铁循环巨噬细胞的发育
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白介素33信号调控铁循环巨噬细胞的发育

浏览次数:    时间:2020-04-13

本期文章:《免疫》:Online/在线发表

英国剑桥大学Ziad Mallat研究小组发现,白介素33信号调控铁循环巨噬细胞的发育。相关论文于2020年4月8日在线发表在《免疫》杂志上。

研究人员证明,白细胞介素(IL)-33与红细胞相关并与血红素共同作用,通过激活MyD88衔接蛋白和IL-33受体IL1RL1下游的ERK1/2激酶来促进成熟红髓巨噬细胞(RPM)的生成。缺乏IL-33和IL1RL1的小鼠显示出不良的铁循环并增加了脾脏的铁沉积。

 

基因表达和染色质可及性研究表明,在RPM前体(保留了分化为RPM的全部潜力)的发育过程中,IL-33信号下游的GATA转录因子发挥了作用。

 

因此,IL-33指导RPM的发育,从而作为对生理性红细胞损伤的反应,这些研究对铁的循环利用和铁的稳态具有重要意义。

 

据介绍,脾脏的RPM有助于红细胞的动态平衡,并且是铁循环所必需的。血红素诱导单核细胞来源的巨噬细胞中SPIC转录因子的表达,并促进其分化为RPM前体(pre-RPM)。但是,分化为成熟RPM的要求仍然未知。

 

附:英文原文

Title: Interleukin-33 Signaling Controls the Development of Iron-Recycling Macrophages

Author: Yuning Lu, Gemma Basatemur, Ian C. Scott, Davide Chiarugi, Marc Clement, James Harrison, Ravin Jugdaohsingh, Xian Yu, Stephen A. Newland, Helen E. Jolin, Xuan Li, Xiao Chen, Monika Szymanska, Guttorm Haraldsen, Gaby Palmer, Padraic G. Fallon, E. Suzanne Cohen, Andrew N.J. McKenzie, Ziad Mallat

Issue&Volume: 2020-04-08

Abstract: Splenic red pulp macrophages (RPMs) contribute to erythrocyte homeostasis and are required for iron recycling. Heme induces the expression of SPIC transcription factor in monocyte-derived macrophages and promotes their differentiation into RPM precursors, pre-RPMs. However, the requirements for differentiation into mature RPMs remain unknown. Here, we have demonstrated that interleukin (IL)-33 associated with erythrocytes and co-cooperated with heme to promote the generation of mature RPMs through activation of the MyD88 adaptor protein and ERK1/2 kinases downstream of the IL-33 receptor, IL1RL1. IL-33- and IL1RL1-deficient mice showed defective iron recycling and increased splenic iron deposition. Gene expression and chromatin accessibility studies revealed a role for GATA transcription factors downstream of IL-33 signaling during the development of pre-RPMs that retained full potential to differentiate into RPMs. Thus, IL-33 instructs the development of RPMs as a response to physiological erythrocyte damage with important implications to iron recycling and iron homeostasis.

DOI: 10.1016/j.immuni.2020.03.006

Source: https://www.cell.com/immunity/fulltext/S1074-7613(20)30119-9

期刊信息

Immunity:《免疫》,创刊于1994年。隶属于细胞出版社,最新if:21.522
官方网址:https://www.cell.com/immunity/home
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