Karwaciak Iwona, Sałkowska Anna, Karaś Kaja, Dastych Jarosław, Ratajewski Marcin
Laboratory of Transcriptional Regulation, Institute of Medical Biology, Polish Academy of Sciences, 93-232 Lodz, Poland.
Laboratory of Epigenetics, Institute of Medical Biology, Polish Academy of Sciences, 93-232 Lodz, Poland.
Vaccines (Basel). 2021 Jan 15;9(1):54. doi: 10.3390/vaccines9010054.
The pandemic of the new coronavirus SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) has led to the deaths of more than 1.5 million people worldwide. SARS-CoV-2 causes COVID-19, which exhibits wide variation in the course of disease in different people, ranging from asymptomatic and mild courses to very severe courses that can result in respiratory failure and death. Despite the rapid progression of knowledge, we still do not know how individual cells of the immune system interact with the virus or its components, or how immune homeostasis becomes disrupted, leading to the rapid deterioration of a patient's condition. In the present work, we show that SARS-CoV-2 proteins induce the expression and secretion of IL-6 by human monocytes and macrophages, the first line cells of antiviral immune responses. IL-6 may play a negative role in the course of COVID-19 by inhibiting Th1-dependent immunity and stimulating Th17 lymphocytes, thus leading to an increased probability of a cytokine storm.
新型冠状病毒SARS-CoV-2（严重急性呼吸综合征冠状病毒2）大流行已导致全球超过150万人死亡。SARS-CoV-2引发新冠肺炎，该病在不同人群中的病程表现出很大差异，从无症状和轻症病程到可能导致呼吸衰竭和死亡的非常严重的病程。尽管知识进展迅速，但我们仍然不知道免疫系统的单个细胞如何与病毒或其成分相互作用，或者免疫稳态如何被破坏，从而导致患者病情迅速恶化。在本研究中，我们表明SARS-CoV-2蛋白可诱导人类单核细胞和巨噬细胞（抗病毒免疫反应的一线细胞）表达和分泌白细胞介素-6（IL-6）。IL-6可能通过抑制Th1依赖性免疫和刺激Th17淋巴细胞在新冠肺炎病程中发挥负面作用，从而导致细胞因子风暴的可能性增加。
