The Wistar Institute, Philadelphia, Pennsylvania, USA.
Key Laboratory of Immune Microenvironment and Disease of the Ministry of Education, Department of Immunology, School of Basic Sciences, Tianjin Medical University, Tianjin, China.
J Leukoc Biol. 2022 Nov;112(5):955-968. doi: 10.1002/JLB.4HI0921-514RR. Epub 2022 Jun 21.
Transitory appearance of immune suppressive polymorphonuclear neutrophils (PMNs) defined as myeloid-derived suppressor cells (PMNs-MDSCs) in newborns is important for their protection from inflammation associated with newly established gut microbiota. Here, we report that inhibition of the type I IFN (IFN1) pathway played a major role in regulation of PMNs-MDSCs-suppressive activity during first weeks of life. Expression of the IFN1 receptor IFNAR1 was markedly lower in PMNs-MDSCs. However, in newborn mice, down-regulation of IFNAR1 was not sufficient to render PMNs immune suppressive. That also required the presence of a positive signal from lactoferrin via its receptor low-density lipoprotein receptor-related protein 2. The latter effect was mediated via NF-κB activation, which was tempered by IFN1 in a manner that involved suppressor of cytokine signaling 3. Thus, we discovered a mechanism of tight regulation of immune suppressive PMNs-MDSCs in newborns, which may be used in the development of therapies of neonatal pathologies.
新生儿中短暂出现的免疫抑制性多形核粒细胞(PMN)被定义为髓系来源的抑制细胞(PMN-MDSC),对于它们免受与新建立的肠道微生物群相关的炎症的保护至关重要。在这里,我们报告称,I 型 IFN(IFN1)途径的抑制在生命最初几周PMN-MDSC 抑制活性的调节中起着主要作用。PMN-MDSC 中 IFN1 受体 IFNAR1 的表达明显降低。然而,在新生小鼠中,IFNAR1 的下调不足以使 PMN 具有免疫抑制性。这还需要乳铁蛋白通过其受体低密度脂蛋白受体相关蛋白 2 提供阳性信号。这种效应是通过 NF-κB 激活介导的,IFN1 以涉及细胞因子信号转导抑制因子 3 的方式对其进行调节。因此,我们发现了一种严格调节新生儿免疫抑制性 PMN-MDSC 的机制,这可能用于开发新生儿疾病的治疗方法。