Vomero Marta, Barbati Cristiana, Colasanti Tania, Celia Alessandra Ida, Speziali Mariangela, Ucci Federica Maria, Ciancarella Claudia, Conti Fabrizio, Alessandri Cristiano
Rheumatology Unit, Department of Clinical, Internal, Anesthesiological and Cardiovascular Sciences, Sapienza University of Rome, Rome, Italy.
Front Pharmacol. 2020 Nov 19;11:569849. doi: 10.3389/fphar.2020.569849. eCollection 2020.
Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) is the novel coronavirus, causing coronavirus disease 2019 (COVID-19). During virus infection, several pro-inflammatory cytokines are produced, leading to the "cytokine storm." Among these, interleukin (IL)-6, tumor necrosis factor-α (TNF-α), and IL-1β seem to have a central role in the progression and exacerbation of the disease, leading to the recruitment of immune cells to infection sites. Autophagy is an evolutionarily conserved lysosomal degradation pathway involved in different aspects of lymphocytes functionality. The involvement of IL-6, TNF-α, and IL-1β in autophagy modulation has recently been demonstrated. Moreover, preliminary studies showed that SARS-CoV-2 could infect lymphocytes, playing a role in the modulation of autophagy. Several anti-rheumatic drugs, now proposed for the treatment of COVID-19, could modulate autophagy in lymphocytes, highlighting the therapeutic potential of targeting autophagy in SARS-CoV-2 infection.
严重急性呼吸综合征冠状病毒2（SARS-CoV-2）是一种新型冠状病毒，可引发2019冠状病毒病（COVID-19）。在病毒感染期间，会产生几种促炎细胞因子，导致“细胞因子风暴”。其中，白细胞介素（IL）-6、肿瘤坏死因子-α（TNF-α）和IL-1β似乎在疾病的进展和加重过程中起核心作用，导致免疫细胞募集到感染部位。自噬是一种进化上保守的溶酶体降解途径，参与淋巴细胞功能的不同方面。最近已证实IL-6、TNF-α和IL-1β参与自噬调节。此外，初步研究表明，SARS-CoV-2可感染淋巴细胞，在自噬调节中发挥作用。目前提议用于治疗COVID-19的几种抗风湿药物可调节淋巴细胞中的自噬，突出了针对SARS-CoV-2感染中的自噬进行治疗的潜力。
