Depletion and Dysfunction of Dendritic Cells: Understanding SARS-CoV-2 Infection

Uncontrolled severe acute respiratory syndrome-coronavirus (SARS-CoV)-2 infection is closely related to disorders of the innate immune and delayed adaptive immune systems. Dendritic cells (DCs) bridge innate immunity and adaptive immunity. DCs have important roles in defending against SARS-CoV-2 infection. In this review, we summarize the latest research concerning the role of DCs in SARS-CoV-2 infection. We focus on the complex interplay between DCs and SARS-CoV-2: pyroptosis-induced activation; activation of the renin-angiotensin-aldosterone system; and activation of dendritic cell-specific intercellular adhesion molecule 3-grabbing non-integrin. We also discuss the decline in DC number, the impaired antigen-presentation capability, and the reduced production of type-I interferon of DCs in severe SARS-CoV-2 infection. In addition, we discuss the potential mechanisms for pathological activation of DCs to understand the pattern of SARS-CoV-2 infection. Lastly, we provide a brief overview of novel vaccination and immunotherapy strategies based on DC targeting to overcome SARS-CoV-2 infection.

Automated summary

This review summarizes the latest research on the role of dendritic cells (DCs) in SARS-CoV-2 infection, including their interaction with pyroptosis-induced activation, the renin-angiotensin-aldosterone system, and dendritic cell-specific intercellular adhesion molecule 3-grabbing non-integrin. The review also discusses the reduction in DC number, impaired antigen-presentation capability, and decreased production of type-I interferon in severe SARS-CoV-2 infection. Additionally, potential mechanisms for pathological activation of DCs to understand the pattern of SARS-CoV-2 infection are explored, followed by a brief overview of novel vaccination and immunotherapy strategies based on DC targeting to overcome SARS-CoV-2 infection.