Type I Interferon Induction and Exhaustion during Viral Infection: Plasmacytoid Dendritic Cells and Emerging COVID-19 Findings

Greene, Trever T; Zúñiga, Elina I.

doi:10.3390/v13091839

Cited by 23 publications

(19 citation statements)

References 170 publications

(281 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Genetic defects observed in critically ill COVID-19 patients are acquired during disease evolution through secondary events, in deficient pDCs. Despite this, the specific role of DCs in the COVID-19 pathology has been insufficiently studied, so far [ 55 , 84 ].…”

Section: Discussionmentioning

confidence: 99%

Innate immunity to SARS-CoV-2 infection: a review

et al. 2022

View full text Add to dashboard Cite

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic, first notified in China, has spread around the world causing high morbidity and mortality, which is due to factors such as the subversion of the immune response. The aims of the study are to summarise and present the immunopathological relationship of COVID-19 with innate immunity. This is a systematic review conducted by the National Library of Medicine -National Institutes of Health, USA (PUBMED), Latin American and Caribbean Literature on Health Sciences (LILACS), Medical Literature Analysis and Retrieval System Online (MEDLINE) and Scientific Electronic Library Online (SCIELO) databases with clinical trials, in vitro assays, case-controls, cohort studies, systematic reviews and meta-analyses between February 2020 and July 2021. The version 2 of the Cochrane risk-of-bias tool for RCTs (RoB 2), Joana Briggs Institute (JBI) Critical Appraisal (for the review articles) and the Risk of Bias in Non-randomised Studies of Interventions (ROBINS-I) tools were used to evaluate the quality and the risk of bias of the studies included in this review. The innate immune response through the generation of interferons, alternative pathways and complement system lectins and the joint action of innate immune cells and cytokines and chemokines lead to different clinical outcomes, taking into account the exacerbated inflammatory response and pathogenesis. Then, in addition to interacting as a bridge for adaptive immunity, the innate immune response plays an essential role in primary defense and is one of the starting points for immune evasion by SARS-CoV-2.

show abstract

Section: Discussionmentioning

confidence: 99%

Innate immunity to SARS-CoV-2 infection: a review

et al. 2022

View full text Add to dashboard Cite

show abstract

“…However, exhausted T cells are still important for controlling the host–pathogen equilibrium in a chronic infection ( Schmitz et al., 1999 ). In addition to the T-cell compartment, the innate immune system is affected during chronic infections ( Zuniga et al., 2015 ; Greene and Zuniga, 2021 ). The complement system, which is a key effector of innate immune responses in acute infections, has also been shown to be involved in the modulation of adaptive immune responses ( Ricklin et al., 2010 ).…”

Section: Introductionmentioning

confidence: 99%

Role of the Complement System in the Modulation of T-Cell Responses in Chronic Chagas Disease

Caputo¹,

Elias²,

Cesar³

et al. 2022

Front. Cell. Infect. Microbiol.

View full text Add to dashboard Cite

Chagas disease, caused by the intracellular pathogen Trypanosoma cruzi, is the parasitic disease with the greatest impact in Latin America and the most common cause of infectious myocarditis in the world. The immune system plays a central role in the control of T. cruzi infection but at the same time needs to be controlled to prevent the development of pathology in the host. It has been shown that persistent infection with T. cruzi induces exhaustion of parasite-specific T cell responses in subjects with chronic Chagas disease. The continuous inflammatory reaction due to parasite persistence in the heart also leads to necrosis and fibrosis. The complement system is a key element of the innate immune system, but recent findings have also shown that the interaction between its components and immune cell receptors might modulate several functions of the adaptive immune system. Moreover, the findings that most of immune cells can produce complement proteins and express their receptors have led to the notion that the complement system also has non canonical functions in the T cell. During human infection by T. cruzi, complement activation might play a dual role in the acute and chronic phases of Chagas disease; it is initially crucial in controlling parasitemia and might later contributes to the development of symptomatic forms of Chagas disease due to its role in T-cell regulation. Herein, we will discuss the putative role of effector complement molecules on T-cell immune exhaustion during chronic human T. cruzi infection.

show abstract

“…IFN‐I responses are critical in COVID‐19, as indicated by 15–20% of severely diseased patients showing inborn errors of IFN‐I immunity or autoantibodies against IFN‐I (Zhang et al , 2022 ). In early stages of COVID‐19, reduced IFN‐I and enhanced TNFα and IL‐6 responses are associated with increased disease severity, whereas diminished IFN‐I production is correlated with decreased function and numbers of peripheral blood pDC (reviewed in Greene & Zuniga, 2021 ). In later disease stages, excessive IFN‐I responses or treatment with exogenous IFN‐I can be detrimental (Greene & Zuniga, 2021 ).…”

mentioning

confidence: 99%

“…In early stages of COVID‐19, reduced IFN‐I and enhanced TNFα and IL‐6 responses are associated with increased disease severity, whereas diminished IFN‐I production is correlated with decreased function and numbers of peripheral blood pDC (reviewed in Greene & Zuniga, 2021 ). In later disease stages, excessive IFN‐I responses or treatment with exogenous IFN‐I can be detrimental (Greene & Zuniga, 2021 ). In line with this, also van der Sluis et al ( 2022 ) found reduced numbers of blood pDC in hospitalized COVID‐19 patients and the extent of pDC reduction correlated with disease severity and with high flow oxygen supplementation.…”

mentioning

confidence: 99%

“…Consistently, in blood‐derived pDC, the SARS‐CoV‐2 envelope protein induced IL‐6, but not IFN‐I expression (Fig 1B ). So far, TLR2‐dependent responses of pDC were rarely studied, and TLR2 was more discussed in the context of bacterial pDC stimulation, for example, as a sensor of components from commensal bacteria that render pDC tolerogenic (reviewed in Reizis, 2019 and Greene & Zuniga, 2021 ).…”

mentioning

confidence: 99%

See 1 more Smart Citation

Toll‐like receptors matter: plasmacytoid dendritic cells in COVID‐19

Becker

Kalinke

2022

The EMBO Journal

View full text Add to dashboard Cite

Plasmacytoid dendritic cells (pDC) have the unique ability to rapidly mount high‐level antiviral type I interferon (IFN‐I) responses during diverse virus infections. In COVID‐19 patients, reduced pDC numbers correlate with diminished IFN‐I serum levels and enhanced disease severity. However, the molecular mechanisms underlying SARS‐CoV‐2‐mediated pDC stimulation to induce cytokine responses are still largely unclear. In this issue of the EMBO Journal, van der Sluis and colleagues tackled this question by using an innovative hematopoietic stem and progenitor cells (HSPC)‐pDC system that allows gene editing and the detailed analysis of pDC sensing mechanisms.

show abstract

Type I Interferon Induction and Exhaustion during Viral Infection: Plasmacytoid Dendritic Cells and Emerging COVID-19 Findings

Cited by 23 publications

References 170 publications

Innate immunity to SARS-CoV-2 infection: a review

Innate immunity to SARS-CoV-2 infection: a review

Role of the Complement System in the Modulation of T-Cell Responses in Chronic Chagas Disease

Toll‐like receptors matter: plasmacytoid dendritic cells in COVID‐19

Contact Info

Product

Resources

About