MafB是巨噬细胞发育和跨组织和物种功能特性的保守转录调节因子，这一成果由里昂大学Thomas Marichal团队经过不懈努力而取得。2026年2月26日出版的《免疫学》杂志发表了这一最新研究成果。

研究组发现，骨髓源性巨噬细胞（BMDMs）和大多数RTMs在体内的发育需要MafB。在CD52高的未成熟阶段，MafB缺乏保留了RTM，破坏了整体和组织特异性的身份和功能，损害了吞噬作用、脾铁循环以及肺、肾和肠道生理。表观遗传分析显示，MafB直接调控小鼠和人类的关键RTM基因，包括Csf1r、Mertk、Fcgr1、Cd163和Zeb2。计算机分析进一步证明了脊椎动物中MafB结合位点的进化保守性。总之，这些发现确定了MafB是RTM发育和功能认同的关键调节因子，将依赖MafB的转录程序与RTM的定义特征和组织稳态联系起来。

据了解，稳态常驻组织巨噬细胞（RTMs）不仅在组织中表现出多样性，而且在保守的转录程序驱动下具有共同的特征。虽然转录因子MafB在巨噬细胞中高表达，但其在建立RTM身份和功能中的作用尚不清楚。

附：英文原文

Title: MafB is a conserved transcriptional regulator of macrophage development and functional identity across tissues and species

Author: Domien Vanneste, Wen Peng, Zhuangzhuang Liu, Malik Hamadia, Raphal La Rocca, Joan Abinet, Alexis Balthazar, Fabienne Perin, Alexandre Hego, Didier Cataldo, Fabrice Bureau, Philippe Compère, Bénédicte Machiels, Charlotte L. Scott, Coraline Radermecker, Thomas Marichal

Issue&Volume: 2026-02-26

Abstract: Homeostatic resident tissue macrophages (RTMs) not only exhibit diversity across tissues but also share common features that are driven by conserved transcriptional programs. While the transcription factor MafB is highly expressed in macrophages, its role in establishing RTM identity and functions remains unclear. Here, we show that MafB was required for the development of bone-marrow-derived macrophages (BMDMs) and most RTMs in vivo. MafB deficiency retained RTMs in a CD52high immature stage and disrupted global and tissue-specific identities and functions, impairing phagocytosis, splenic iron recycling, and lung, kidney, and gut physiology. Epigenetic profiling revealed that MafB directly regulated key RTM genes in mice and humans, including Csf1r, Mertk, Fcgr1, Cd163, and Zeb2. In silico analyses further demonstrated strong evolutionary conservation of MafB binding sites across vertebrates. Together, these findings establish MafB as a crucial regulator of RTM development and functional identity, linking MafB-dependent transcriptional programs with defining features of RTMs and tissue homeostasis.

DOI: 10.1016/j.immuni.2026.01.012

Source: https://www.cell.com/immunity/abstract/S1074-7613(26)00033-6