Department of Histology, Faculty of Medicine, Universitas Indonesia, Jakarta Pusat, Indonesia; Immunology, Master's Program in Biomedical Sciences, Faculty of Medicine, Universitas Indonesia, Jakarta Pusat, Indonesia; Division of Metabolic, Endocrinology and Diabetes, Department of Internal Medicine, Faculty of Medicine, Universitas Indonesia, Jakarta Pusat, Indonesia
Khaedir, Y., Department of Histology, Faculty of Medicine, Universitas Indonesia, Jakarta Pusat, Indonesia, Immunology, Master's Program in Biomedical Sciences, Faculty of Medicine, Universitas Indonesia, Jakarta Pusat, Indonesia; Kartika, R., Division of Metabolic, Endocrinology and Diabetes, Department of Internal Medicine, Faculty of Medicine, Universitas Indonesia, Jakarta Pusat, Indonesia
Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and has been a major threat to global public health. In Indonesia, the cases have rapidly increased, and the case fatality rate remains high. With COVID-19, most of the deaths have been caused by acute respiratory distress syndrome and dysregulation of the immune response. A lung biopsy from a patient with COVID-19 showed inflammatory cellular infiltration with diffuse alveolar damage. Massive pulmonary destruction has also been reported as a result of highly increased levels of proinflammatory cytokines, such as tumor necrosis factor-? (TNF-?), interleukin-6 (IL-6), IL-1?, interferon-?(IFN-?), induced protein 10 (IP-10), and monocyte chemoattractant protein-1 (MCP-1). IL-6 is an inflammatory cytokine produced by various cell types, including immune cells and nonleukocytes, such as endothelial cells, fibroblasts, epithelial cells, type II pneumocytes, and certain tumor cells. Several studies have shown that IL-6 contributes to the severity and mortality of COVID-19. In this review, we would like to explore the immune response in COVID-19 and the role of IL-6 in the immunopathogenesis of COVID-19. ? Copyright 2021, Mary Ann Liebert, Inc., publishers 2021.