Abstract
Antigen Presenting Cells (APC) are immune cells that recognize, process, and present antigens to lymphocytes. APCs are among the earliest immune responders against an antigen. Thus, in patients with COVID-19, a disease caused by the newly reported SARS-CoV-2 virus, the role of APCs becomes increasingly important. In this paper, we dissect the role of these cells in the fight against SARS-CoV-2. Interestingly, this virus appears to cause a higher mortality among adults than children. This may suggest that the immune system, particularly APCs, of children may be different from that of adults, which may then explain differences in immune responses between these two populations, evident as different pathological outcome. However, the underlying molecular mechanisms that differentiate juvenile from other APCs are not well understood. Whether juvenile APCs are one reason why children are less susceptible to SARS-CoV-2 requires much attention. The goal of this review is to examine the role of APCs, both in adults and children. The molecular mechanisms governing APCs, especially against SARS-CoV-2, may explain the differential immune responsiveness in the two populations.
Highlights
In December 2019, several cases of pneumonia with unknown etiology were identified in Wuhan, China
World Health Organization announced that Severe Acute Respiratory Syndrome (SARS)-CoV-2 was causing the disease Coronavirus Disease (COVID-19), considered a pandemic
During the early stage of infection, by overcoming IFN responses, SARS-CoV-2 promotes its dissemination and the continuous stimulus of an hyper-inflammatory innate immune response [61]. This is responsible for the pathophysiology of COVID-19, whose main symptom is a high titer of pro-inflammatory cytokines
Summary
In December 2019, several cases of pneumonia with unknown etiology were identified in Wuhan, China. World Health Organization announced that SARS-CoV-2 was causing the disease Coronavirus Disease (COVID-19), considered a pandemic This disease is characterized by respiratory tract infections that, depending on the severity, can precipitate acute respiratory stress disorder. This increase in Ca2+ concentration in the ERGIC could activate NLRP3 inflammasome [10], which is a multiprotein complex that induces an inflammatory form of cell death and the release of pro-inflammatory cytokines, as IL-1β This latter is critical for the host response to infections, and can trigger an autoinflammatory loop that promotes the typical COVID-19 hyper-inflammatory status [11,12]. Once inside the host cell, the viral that are exploited by SARS-CoV-2 viral spike (S) protein for its entry. M proteins combine with the nucleocapsid, assembling a mature virion that is secreted from the cell via exocytosis
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