NRG4-ErbB4 信号抑制促炎巨噬细胞活性。
NRG4-ErbB4 signaling represses proinflammatory macrophage activity.
机构信息
The Saban Research Institute, Children's Hospital Los Angeles, Los Angeles, California.
Department of Pediatrics, Keck School of Medicine, University of Southern California, Los Angeles, California.
出版信息
Am J Physiol Gastrointest Liver Physiol. 2021 Jun 1;320(6):G990-G1001. doi: 10.1152/ajpgi.00296.2020. Epub 2021 Apr 7.
Proinflammatory macrophages are essential drivers of colitis and express the growth factor receptor ErbB4. This study tested the role of ErbB4 and its specific ligand, NRG4, in regulating macrophage function. We show that endogenous NRG4-ErbB4 signaling limits macrophage production of proinflammatory cytokines in vitro and limits colitis severity in vivo and thus is a potential target for therapeutic intervention.
促炎性巨噬细胞是结肠炎的主要驱动因素，并且表达生长因子受体 ErbB4。本研究检测了 ErbB4 及其特定配体 NRG4 在调节巨噬细胞功能中的作用。我们表明，内源性 NRG4-ErbB4 信号限制了体外巨噬细胞产生促炎细胞因子的能力，并限制了体内结肠炎的严重程度，因此是治疗干预的潜在靶点。
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