Immunobiology and immunotherapy of COVID-19: A clinically updated overview

Abstract

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a new member of the coronavirus family that can cause coronavirus disease 2019 (COVID-19). COVID-9 has become a global pandemic with severe health issues around the world. Identifying the accurate immunopathogenesis of the COVID-19 and the immune response against SARS-CoV-2 is necessary for the development of therapeutic approaches and rational drug design. This paper aims to overview the updated clinical data on the immunopathogenesis of the COVID-19 and review the innate and adaptive immune response to SARS-CoV-2. Also, challenges of the immune response to SARS-CoV-2 leading to dysfunctional immune response and their contribution to the progression of the disease have been discussed. To achieve a more efficient immune response, multiple methods could be applied, including regulation of the immune response, augmentation of the immune system against the virus, inhibition of the dysfunctional immune checkpoints, and inhibition of the viral replication/infection. Based on the immune response against SARS-CoV-2 and its dysfunction, we introduce potential immunotherapies as well as reviewing recruiting/completed clinical trials of COVID-19.

Keywords: COVID-19; SARS-CoV-2; clinical trial; immunopathogenesis; immunotherapy.

Figure 1

Immunotherapeutic approaches for COVID‐19. (Created by Esmaeilzadeh et al.) aAPC, artificial antigen‐presenting cell; BCG, Bacille Calmette–Guérin; CAR NK cell, chimeric antigen receptor natural killer cell; CCR5, CC chemokine receptor 5; CD14, cluster of differentiation 14; DC, dendritic cell; DNA, deoxyribonucleic acid; GM‐CSF, granulocyte‐macrophage colony‐stimulating factor; IFN‐γ, interferon‐γ; IL, interleukin; IVIG, intravenous immunoglobulin; JAK, Jasus kinase; MSC, mesenchymal stem cell; NK cell, natural killer cell; PD‐1, programmed death‐1; RNA, ribonucleic acid; Tim‐3, T‐cell immunoglobulin and mucin‐domain containing‐3; TNF, tumor necrosis factor; VEGF, vascular endothelial growth factor