The role of antigen-presenting cells in the pathogenesis of COVID-19

Farzi, Rana; Aghbash, Parisa Shiri; Eslami, Narges; Azadi, Arman; Shamekh, Ali; Hemmat, Nima; Entezari‐Maleki, Taher; Baghi, Hossein Bannazadeh

doi:10.1016/j.prp.2022.153848

Cited by 25 publications

(14 citation statements)

References 164 publications

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“…During SARS-CoV-2 infection, DCs are the leading producers of main pro-inflammatory cytokines, and they can release type I and type III IFNs, which help to achieve a sustained antiviral state that limits the viral spread and suppress the viral infection [ 26 ]. A decrease in circulating myeloid (CD11c+CD123lo/-) and plasmacytoid (CD11c–CD123+) DCs was noted in severely ill COVID-19 patients [ 27 , 28 , 29 ] ( Figure 1 ).…”

Section: Antigen-presenting Cells In Covid-19mentioning

confidence: 99%

Dysregulated Immune Responses in SARS-CoV-2-Infected Patients: A Comprehensive Overview

Kudryavtsev

Rubinstein

Головкин

et al. 2022

Viruses

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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was first detected in humans more than two years ago and caused an unprecedented socio-economic burden on all countries around the world. Since then, numerous studies have attempted to identify various mechanisms involved in the alterations of innate and adaptive immunity in COVID-19 patients, with the ultimate goal of finding ways to correct pathological changes and improve disease outcomes. State-of-the-art research methods made it possible to establish precise molecular mechanisms which the new virus uses to trigger multisystem inflammatory syndrome and evade host antiviral immune responses. In this review, we present a comprehensive analysis of published data that provide insight into pathological changes in T and B cell subsets and their phenotypes, accompanying the acute phase of the SARS-CoV-2 infection. This knowledge might help reveal new biomarkers that can be utilized to recognize case severity early as well as to provide additional objective information on the effective formation of SARS-CoV-2-specific immunity and predict long-term complications of COVID-19, including a large variety of symptoms termed the ‘post-COVID-19 syndrome’.

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Section: Antigen-presenting Cells In Covid-19mentioning

confidence: 99%

Dysregulated Immune Responses in SARS-CoV-2-Infected Patients: A Comprehensive Overview

Kudryavtsev

Rubinstein

Головкин

et al. 2022

Viruses

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“…It develops as a result of host immune response dysfunction, activation of the coagulation cascade, and subsequent medium artery thrombosis [ 34 ]. Additionally, it has been demonstrated by histology and immunohistochemical investigations that gallbladder vasculitis, as well as endothelial overexpression of medium-sized arteries, increased CD4 T cells, and excessively elevated macrophage frequencies, contributes to gallbladder endothelial dysfunction [ 35 , 36 ]. The pathophysiological processes are controversial despite several studies in this area.…”

Section: The Hypothesis In the Pathogenesis Of Covid-19's Liver Damagementioning

confidence: 99%

Hepatic Disorders and COVID-19: From Pathophysiology to Treatment Strategy

Aghbash

Leylabadlo

Fathi

et al. 2022

Canadian Journal of Gastroenterology and Hepatology

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Following the SARS-CoV-2 outbreak and the subsequent development of the COVID-19 pandemic, organs such as the lungs, kidneys, liver, heart, and brain have been identified as priority organs. Liver diseases are considered a risk factor for high mortality from the COVID-19 pandemic. Besides, liver damage has been demonstrated in a substantial proportion of patients with COVID-19, especially those with severe clinical symptoms. Furthermore, antiviral medications, immunosuppressive drugs after liver transplantation, pre-existing hepatic diseases, and chronic liver diseases such as cirrhosis have also been implicated in SARS-CoV-2-induced liver injury. As a result, some precautions have been taken to prevent, monitor the virus, and avoid immunocompromised and susceptible individuals, such as liver and kidney transplant recipients, from being infected with SARS-CoV-2, thereby avoiding an increase in mortality. The purpose of this review was to examine the impairment caused by SARS-CoV-2 infection and the impact of drugs used during the pandemic on the mortality range and therefore the possibility of preventive measures in patients with liver disease.

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“…Activated fibroblasts and endothelial cells at the BBB lining are also implicated in BBB disruption, causing increased BBB permeability and permitting the transmigration of (auto)antibodies, cytokines and activated immune cells in the subarachnoid space. Within the subarachnoid space, T cells can be reactivated by antigen-presenting cells ( 78 ). Within the brain tissue, a limited presence of SARS-CoV-2 spike protein or viral particles is hypothesized in LCS; thus, neurovirulence is probably not strongly associated with LCS pathophysiology ( 79 ).…”

Section: Figurementioning

confidence: 99%

New‑onset neuropsychiatric sequelae and ‘long‑COVID’ syndrome (Review)

et al. 2022

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The ongoing coronavirus disease 2019 (COVID-19) pandemic has had a widespread impact on individuals' mental health through indirect psychological and social mechanisms, related to factors such as fear of infection or death, social isolation, lack of social support and financial instability. The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection has also been associated with the development or recurrence of neuropsychiatric symptoms, both during the acute phase, as well as during the post-acute 'long-COVID' phase. In addition to the COVID-19 survivors with a mental health history that are at a high risk of experiencing a range of neuropsychiatric symptoms following resolution of acute COVID-19, there is accumulating evidence that a diagnosis of COVID-19 may also be associated with new-onset neuropsychiatric morbidity among survivors without pre-existing mental health disorders. In particular, studies investigating the incidence of post-acute neuropsychiatric sequelae, based mostly on retrospective cohort study designs and data from national health registries, have reported the development of new-onset manifestations, including depression, anxiety, psychotic symptoms, sleep disturbances and fatigue. Nevertheless, when COVID-19 survivors were compared with SARS-CoV-2-negative controls and especially survivors of other disorders (such as influenza), the findings regarding the risk of incident neuropsychiatric manifestations varied among studies. While there is evidence of an association between SARS-CoV-2 infection and the subsequent occurrence of new-onset neuropsychiatric symptoms, especially among patients with increased disease severity, further research using methodological approaches less susceptible to confounding bias is required to establish causal relationships. Contents 1. Introduction 2. New-onset neuropsychiatric sequelae in COVID-19 survivors 3. Pathophysiological mechanisms and 'long-COVID' neuropsychiatric symptoms 4. Conclusions

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The role of antigen-presenting cells in the pathogenesis of COVID-19

Cited by 25 publications

References 164 publications

Dysregulated Immune Responses in SARS-CoV-2-Infected Patients: A Comprehensive Overview

Dysregulated Immune Responses in SARS-CoV-2-Infected Patients: A Comprehensive Overview

Hepatic Disorders and COVID-19: From Pathophysiology to Treatment Strategy

New‑onset neuropsychiatric sequelae and ‘long‑COVID’ syndrome (Review)

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