Abstract
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.
Highlights
The coronavirus disease 2019 (COVID-19) pandemic poses a serious threat to public health and economic systems worldwide [1]
SARS-CoV-2 infection induces pyroptosis, which leads to release of SARS-CoV-2, pathogen-associated molecular patterns (PAMPs), and damage-associated molecular patterns (DAMPs) [7, 9, 10]
Dendritic cells (DCs) aggregation has been observed in the bronchoalveolar lavage fluid of COVID-19 patients, which suggests that DCs infiltrate into lung tissues by the products of SARS-CoV-2-induced pyroptosis [35,36,37,38] (Figure 1)
Summary
The coronavirus disease 2019 (COVID-19) pandemic poses a serious threat to public health and economic systems worldwide [1]. Pattern recognition receptors (PRRs) expressed on the membrane of DCs, such as Toll-like receptor (TLR), retinoic acid-inducible gene-I, melanoma differentiation-associated protein-5, and the cyclic guanosine monophosphate–adenosine monophosphate synthase–stimulator of interferon genes pathway, can recognize SARS-CoV-2-induced PAMPs and DAMPs [12,13,14] If these receptors are activated, a range of signaling pathways [e.g., interferon regulatory factor 3 (IRF3), IRF7, nuclear factorkappa B (NF-kB)] are activated to regulate proinflammatory cytokines (e.g., tumor necrosis factor a (TNFa), interleukin (IL), monocyte chemoattractant-1, macrophage inflammatory protein (MIP)1a, MIP1b) in the nucleus and induce interferon type I (IFN-I; the main cytokine responsible for producing a strong antiviral response) production [15, 16]. We hope to create a breakthrough in immunomodulation therapy and an IFN strategy against COVID-19
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
