小柯机器人

美国宾夕法尼亚大学George Hajishengallis、德国德累斯顿理工大学Triantafyllos Chavakis等研究人员合作发现，骨髓生成的先天性免疫训练失调与炎症性合并症有关。该研究于2022年4月27日在线发表于国际一流学术期刊《细胞》。

研究人员表示。骨髓（BM）介导的训练的先天免疫（TII），是造血干细胞和祖细胞（HSPC）及其骨髓后代的免疫反应性提高的状态。

研究人员表明，不适应的BM介导的TII是炎症合并症的基础，如牙周炎-关节炎轴的例子。小鼠实验性牙周炎相关的系统性炎症诱发了HSPC的表观遗传学重构，并导致髓系细胞的生产持续增强，炎症准备程度增加。牙周炎诱导的训练表型可通过BM移植到初始的受体上，当受体遭受炎症性关节炎时，表现出更多的炎症反应性和疾病严重性。HSPC中的IL-1信号对其在牙周炎下的适应性训练至关重要。因此，骨髓组织的适应性先天免疫训练是炎症性合并症的基础，可以通过整体方法以药物为靶标来治疗它们。

附：英文原文

Title: Maladaptive innate immune training of myelopoiesis links inflammatory comorbidities

Author: Xiaofei Li, Hui Wang, Xiang Yu, Gundappa Saha, Lydia Kalafati, Charalampos Ioannidis, Ioannis Mitroulis, Mihai G. Netea, Triantafyllos Chavakis, George Hajishengallis

Issue&Volume: 2022-04-27

Abstract: Bone marrow (BM)-mediated trained innate immunity (TII) is a state of heightened immuneresponsiveness of hematopoietic stem and progenitor cells (HSPC) and their myeloidprogeny. We show here that maladaptive BM-mediated TII underlies inflammatory comorbidities,as exemplified by the periodontitis-arthritis axis. Experimental-periodontitis-relatedsystemic inflammation in mice induced epigenetic rewiring of HSPC and led to sustainedenhancement of production of myeloid cells with increased inflammatory preparedness.The periodontitis-induced trained phenotype was transmissible by BM transplantationto naive recipients, which exhibited increased inflammatory responsiveness and diseaseseverity when subjected to inflammatory arthritis. IL-1 signaling in HSPC was essentialfor their maladaptive training by periodontitis. Therefore, maladaptive innate immunetraining of myelopoiesis underlies inflammatory comorbidities and may be pharmacologicallytargeted to treat them via a holistic approach.

DOI: 10.1016/j.cell.2022.03.043

Source: https://www.cell.com/cell/fulltext/S0092-8674(22)00393-2