The Tug-of-War between Dendritic Cells and Human Chronic Viruses

Rahman, Saifur; Khan, Zafar K.; Jain, Pooja

doi:10.3109/08830185.2011.561506

Cited by 9 publications

(9 citation statements)

References 222 publications

(242 reference statements)

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“…When a virus surpasses a species after years of co-evolution, the new host would respond to it with a more severe immune reaction that can even damage host tissues. Accordingly, possible severe immune response to SARS-CoV-2 is expected ( Fung et al, 2020 ; Rahman et al, 2011 ; Wagstaff et al, 2013 ). There are several pathways proposed to be involved in human immune response toward SARS-CoV-2, and all include two general phases, innate and adaptive immune responses ( Fig.…”

Section: Mechanisms Of Cns Involvementmentioning

confidence: 99%

SARS-CoV-2 and nervous system: From pathogenesis to clinical manifestation

Keyhanian

Umeton

Mohit

et al. 2021

Journal of Neuroimmunology

121

146

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Since the coronavirus disease 2019 (COVID-19) pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a growing body of evidence indicates that besides common COVID-19 symptoms, patients may develop various neurological manifestations affecting both the central and peripheral nervous systems as well as skeletal muscles. These manifestations can occur prior, during and even after the onset of COVID-19 general symptoms. In this Review, we discuss the possible neuroimmunological mechanisms underlying the nervous system and skeletal muscle involvement, and viral triggered neuroimmunological conditions associated with SARS-CoV-2, as well as therapeutic approaches that have been considered for these specific complications worldwide.

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Section: Mechanisms Of Cns Involvementmentioning

confidence: 99%

SARS-CoV-2 and nervous system: From pathogenesis to clinical manifestation

Keyhanian

Umeton

Mohit

et al. 2021

Journal of Neuroimmunology

121

146

View full text Add to dashboard Cite

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“…This work was financially supported by the National Research Projects (PRIN 2010-2011 and Ex-60%) from MIUR (Ministero Istruzione, Università e Ricerca) and by the FP7 project HLH-Cure.…”

Section: Acknowledgmentsmentioning

confidence: 99%

Interferon-α Production by Plasmacytoid Dendritic Cells Is Dispensable for an Effective Anti-Cytomegalovirus Response in Adaptor Protein-3-Deficient Mice

Prete

Luganini

Scutera³

et al. 2015

Journal of Interferon & Cytokine Research

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Adaptor protein-3 (AP-3) is a heterotetrameric complex, which regulates vesicular trafficking. Mutations of the b3A subunit cause the Hermansky-Pudlak syndrome type 2 (HPS-2), a rare genetic disease characterized by albinism, platelet defects, and recurrent infections. Likewise, pearl mice, which lack functional AP-3, show several HPS-2 defects. The AP-3 absence results in defective toll-like receptor trafficking and signaling in dendritic cells (DC), but its effect on the efficiency of the in vivo antiviral response is unclear. We evaluated the impact of AP-3 deficiency on the distribution of DC subsets, interferon (IFN) production, and the susceptibility to murine cytomegalovirus (MCMV) infection. Pearl mice showed a distribution and frequency of conventional (cDC) and plasmacytoid DC (pDC) similar to that of wild-type mice both before and after MCMV infection. Moreover, pearl mice controlled MCMV infection even at high virus doses and showed a normal production of IFN-a. Since pDC, but not cDC, from pearl mice showed an impaired IFN-a and tumor necrosis factor-a production in response to prototypic DNA (MCMV and Herpes Simplex virus) or RNA (Vesicular Stomatitis virus) viruses in vitro, it is likely that MCMV infection can be controlled in vivo independently of an efficient production of IFN-a by pDC, and that the AP-3 complex has a minimal impact on protective antiviral responses.

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“…Viruses, such as HIV, Ebola virus, Respiratory syncytial Virus, and Influenza A virus infect macrophages causing phenotypic changes in these cells that contribute to disease (Mercer and Greber, 2013). Moreover, these viruses can persist in macrophages resulting in virus dissemination, thereby causing recurring pathogenesis (Rahman, et al, 2011). IFN-γ secreted by T cells and NK cells during virus infections triggers innate antiviral immune responses through the IFN-γ receptor (IFNGR) of macrophages.…”

Section: Introductionmentioning

confidence: 99%

Interferon regulatory factor 3 plays a role in macrophage responses to interferon-γ

Guinn

Petro

2019

Immunobiology

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IFN-γ produced during viral infections activates the IFN-γ receptor (IFNGR) complex for STAT1 transcriptional activity leading to expression of Interferon Regulatory Factors (IRF). Simultaneous activation of TBK/IKKε via TLR3 during viral infections activates the transcription factor IRF3. Together these transcription factors contributes to expression of intracellular proteins (e.g. ISG49, ISG54) and secreted proteins (e.g. IFN-β, IP-10, IL-15) that are essential to innate antiviral immunity. Here we examined the role of IRF3 in expression of innate anti-viral proteins produced in response to IFN-γ plus TLR3 agonist. Wild-type (WT) and IRF3KO RAW264.7 cells, each with ISG54-promoter-luciferase reporter vectors, were stimulated with IFN-γ, poly I:C, or both together. ISG54 promoter activity was significantly reduced in IRF3KO RAW264.7 cells responding to IFN-γ, poly I:C, or IFN-γ plus poly I:C, compared with WT RAW264.7 cells. These data were confirmed with western blot and qRT-PCR. Primary macrophages and dendritic cells (DCs) from IRF3KO mice also showed decreased ISG54 in response to IFN-γ, poly I:C, or IFN-γ plus poly I:C compared with those from WT mice. Moreover, pharmacological inhibition of TBK/IKKε significantly reduced ISG54 promoter activity in response to IFN-γ, poly I:C, or IFNγ plus poly I:C. Similarly, expression of ISG49 and IL-15, but not IP-10, was impaired in IRF3KO RAW264.7 cells responding to IFN-γ or poly I:C, which also had impaired STAT1 phosphorylation and IRF1 expression. These data show that IRF3 contributes to IFN-γ/IFNGR signaling for expression of innate anti-viral proteins in macrophages.

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The Tug-of-War between Dendritic Cells and Human Chronic Viruses

Cited by 9 publications

References 222 publications

SARS-CoV-2 and nervous system: From pathogenesis to clinical manifestation

SARS-CoV-2 and nervous system: From pathogenesis to clinical manifestation

Interferon-α Production by Plasmacytoid Dendritic Cells Is Dispensable for an Effective Anti-Cytomegalovirus Response in Adaptor Protein-3-Deficient Mice

Interferon regulatory factor 3 plays a role in macrophage responses to interferon-γ

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