Novartis Institutes for BioMedical Research (NIBR) Translational Medicine, Cambridge, MA, United States.
Novartis Institutes for BioMedical Research (NIBR), Translational Medicine, Basel, Switzerland.
Front Immunol. 2021 Jun 18;12:697405. doi: 10.3389/fimmu.2021.697405. eCollection 2021.
Clinical presentations of COVID-19 are highly variable, yet the precise mechanisms that govern the pathophysiology of different disease courses remain poorly defined. Across the spectrum of disease severity, COVID-19 impairs both innate and adaptive host immune responses by activating innate immune cell recruitment, while resulting in low lymphocyte counts. Recently, several reports have shown that patients with severe COVID-19 exhibit a dysregulated myeloid cell compartment, with increased myeloid-derived suppressor cells (MDSCs) correlating with disease severity. MDSCs, in turn, promote virus survival by suppressing T-cell responses and driving a highly pro-inflammatory state through the secretion of various mediators of immune activation. Here, we summarize the evidence on MDSCs and myeloid cell dysregulation in COVID-19 infection and discuss the potential of MDSCs as biomarkers and therapeutic targets in COVID-19 pneumonia and associated disease.
COVID-19 的临床症状变化多样,但导致不同疾病进程病理生理学的确切机制仍未明确。在疾病严重程度的各个方面,COVID-19 通过激活先天免疫细胞募集,同时导致淋巴细胞计数降低,从而损害固有和适应性宿主免疫反应。最近,有几项报告表明,重症 COVID-19 患者表现出髓样细胞区室失调,髓系来源的抑制细胞(MDSCs)增加与疾病严重程度相关。反过来,MDSCs 通过抑制 T 细胞反应并通过分泌各种免疫激活介质来驱动高度促炎状态,从而促进病毒存活。在这里,我们总结了关于 COVID-19 感染中 MDSCs 和髓样细胞失调的证据,并讨论了 MDSCs 作为 COVID-19 肺炎和相关疾病的生物标志物和治疗靶点的潜力。