Some antibodies can dampen antiviral defences in people with severe COVID

Gentili, Matteo; Hacohen, Nir

doi:10.1038/d41586-021-00352-0

Cited by 2 publications

(4 citation statements)

References 9 publications

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“…During the course of a disease, the characteristics of newly produced antibodies may fine-tune the immune response. One aspect of these changes is an alteration in the antibody Fc component that determines which Fc receptors will be engaged ( Gentili and Hacohen, 2021 ). In this regard, engagement with the Fc receptors CD64, CD16, and CD32 can determine how the immune system combats viral infections.…”

Section: Innate Immunity In Sars-cov-2 Infectionmentioning

confidence: 99%

“…In this regard, engagement with the Fc receptors CD64, CD16, and CD32 can determine how the immune system combats viral infections. Using immune cells from healthy donors exposed to IFN- α and plasma from patients with severe COVID-19, Combes et al individually blocked CD64, CD16, and CD32 Fc receptors and found that CD32 blockade enabled the expression of IFN-regulated genes ( Combes et al, 2021 ; Gentili and Hacohen, 2021 ). Importantly, the CD32 Fc receptor exists in the two forms, CD32A and CD32B, respectively.…”

Section: Innate Immunity In Sars-cov-2 Infectionmentioning

confidence: 99%

“…Importantly, the CD32 Fc receptor exists in the two forms, CD32A and CD32B, respectively. CD32A engagement activates the immune system, whereas CD32B dampens immune responses ( Gentili and Hacohen, 2021 ). Combes and colleagues showed that the inhibition of IFN-regulated genes, including IFITM3 and MX1, in severe COVID-19 cases was due to CD32B engagement.…”

Section: Innate Immunity In Sars-cov-2 Infectionmentioning

confidence: 99%

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The Role of Innate Immunity and Bioactive Lipid Mediators in COVID-19 and Influenza

et al. 2021

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In this review, we discuss spatiotemporal kinetics and inflammatory signatures of innate immune cells specifically found in response to SARS-CoV-2 compared to influenza virus infection. Importantly, we cover the current understanding on the mechanisms by which SARS-CoV-2 may fail to engage a coordinated type I response and instead may lead to exaggerated inflammation and death. This knowledge is central for the understanding of available data on specialized pro-resolving lipid mediators in severe SARS-CoV-2 infection pointing toward inhibited E-series resolvin synthesis in severe cases. By investigating a publicly available RNA-seq database of bronchoalveolar lavage cells from patients affected by COVID-19, we moreover offer insights into the regulation of key enzymes involved in lipid mediator synthesis, critically complementing the current knowledge about the mediator lipidome in severely affected patients. This review finally discusses different potential approaches to sustain the synthesis of 3-PUFA-derived pro-resolving lipid mediators, including resolvins and lipoxins, which may critically aid in the prevention of acute lung injury and death from COVID-19.

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Section: Innate Immunity In Sars-cov-2 Infectionmentioning

confidence: 99%

Section: Innate Immunity In Sars-cov-2 Infectionmentioning

confidence: 99%

Section: Innate Immunity In Sars-cov-2 Infectionmentioning

confidence: 99%

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The Role of Innate Immunity and Bioactive Lipid Mediators in COVID-19 and Influenza

et al. 2021

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“…In this model, we have used a range of IgG titers to spike protein for the simulated data set [52]. However, the role of neutralizing antibodies induced in a large proportion of subjects following natural infection is still being studied [53]. Some subjects do not elicit strong antibody responses.…”

Section: Discussionmentioning

confidence: 99%

Predicting the severity of disease progression in COVID-19 at the individual and population level: A mathematical model

Chirmule,

Nair,

Desai

et al. 2024

Preprint

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The impact of COVID-19 disease on health and economy has been global, and the magnitude of devastation is unparalleled in modern history. Any potential course of action to manage this complex disease requires the systematic and efficient analysis of data that can delineate the underlying pathogenesis. We have developed a mathematical model of disease progression to predict the clinical outcome, utilizing a set of causal factors known to contribute to COVID-19 pathology such as age, comorbidities, and certain viral and immunological parameters. Viral load and selected indicators of a dysfunctional immune response, such as cytokines IL-6 and IFN which contribute to the cytokine storm and fever, parameters of inflammation d-dimer and ferritin, aberrations in lymphocyte number, lymphopenia, and neutralizing antibodies were included for the analysis. The model provides a framework to unravel the multi-factorial complexities of the immune response manifested in SARS-CoV-2 infected individuals. Further, this model can be valuable to predict clinical outcome at an individual level, and to develop strategies for allocating appropriate resources to mitigate severe cases at a population level.

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Some antibodies can dampen antiviral defences in people with severe COVID

Cited by 2 publications

References 9 publications

The Role of Innate Immunity and Bioactive Lipid Mediators in COVID-19 and Influenza

The Role of Innate Immunity and Bioactive Lipid Mediators in COVID-19 and Influenza

Predicting the severity of disease progression in COVID-19 at the individual and population level: A mathematical model

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