The Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) is responsible for the ongoing COVID-19 pandemic, and causes many health complications, including major lung diseases. Besides investigations into the virology of SARS-CoV-2, understanding the immunological routes underlying the clinical manifestations of COVID-19 is important for developing effective therapeutic interventions. The clearance of SARS-CoV-2-infected apoptotic cells by professional efferocytes, through a process termed as ‘efferocytosis’, is essential for maintaining tissue homeostasis, and reducing the chances of health complications caused by SARS-CoV-2 infection. In this review, we focus on the cellular events leading to engagement of the SARS-CoV-2 with type 2 alveolar cells, and how SARS-COV-2 infection impairs the macrophage anti-inflammatory programming. We also discuss accounts of impaired efferocytosis, and the “cytokine storm” which occur concomitantly with the SARS-CoV-2 infection. Finally, we propose how targeting impaired efferocytosis, due to the SARS-CoV-2 infection, may be a beneficial therapeutic strategy to combat COVID-19, and its complications. Graphical Abstract ga1
【저자키워드】 severe acute respiratory syndrome coronavirus 2, Macrophage, ACE2, World Health Organization, adenosine monophosphate; ATP, toll like receptor; TUNNEL, tumour necrosis factor α; TLR, transmembrane serine protease 2; TNF-α, T cell immunoglobulin mucin receptor; TMPRSS2, transforming growth factor beta; TIM, sphingosine-1-phosphate; TGF-β, Suppressor Of Cytokine Signalling; S1P, receptor for advanced glycation end products; SARS-CoV, Phosphatidyl serine; Rac-GEF, milk fat globule-EGF factor 8 protein; PS, Macrophages; MARS-CoV, human coronavirus 229E; HIV, Growth arrest specific gene 6; HCoV229E, food and drug administration; GAS-6, dendritic cell; FDA, cyclooxygenase 2; CXCL, brain angiogenesis inhibitor 1; cAMP, adenosine triphosphate; BAI1, angiotensin-converting enzyme; ARDS, Terminal deoxynucleotidyl transferase dUTP nick end labelling; WHO, Severe acute respiratory syndrome coronavirus 2 infected apoptotic cell; SOCS, SARS-CoV-2-AC, severe acute respiratory syndrome coronavirus; SARS-CoV-2, Rac guanine nucleotide exchange factor; RAGE, proto-oncogene tyrosine-protein kinase MER; MFG-E8, middle east respiratory syndrome-related coronavirus; MERTK, lysophosphatidylcholines;, microtubule-associated protein 1 A/1B-light chain 3; LPC, interleukin; LC3, High mobility group box 1 protein; IL, human immunodeficiency virus; HMGB1, damage associated molecular pattern; DC, chemokine (C-X-C motif) ligand; DAMP, coronavirus disease of 2019; COX2, Chronic obstructive pulmonary disease; COVID-19, cyclic adenosine monophosphate; COPD, acute respiratory distress syndrome; AMP,