NKG2A and COVID-19: another brick in the wall

Antonioli, Luca; Fornai, Matteo; Pellegrini, Carolina; Blandizzi, Corrado

doi:10.1038/s41423-020-0450-7

Cited by 86 publications

(92 citation statements)

References 24 publications

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“…By contrast, those with severe disease are uniquely susceptible to the virus' ability to undermine this response. Specifically, SARS-CoV-2 can suppress IFN induction (Y. Konno, I. Kimura, K. Uriu, M. Fukushi, T. Irie, Y. Koyanagi, S. Nakagawa, and K. Sato, manuscript posted on bioRxiv) and drive IL-6, IL-8, and IL-10 production (24), which to varying degrees inhibits APC maturation (25,26) and upregulates inhibitory receptors on NK and CD8 + T cells (27). Additionally, severe COVID-19 patients have a profound pan lymphopenia characterized by lymphocyte dysfunction, apoptosis, and exhaustion (22,28,29).…”

Section: Covid-19 Immunophenotypesmentioning

confidence: 99%

COVID-19: Complement, Coagulation, and Collateral Damage

Kemper

Woodruff

2020

The Journal of Immunology

147

139

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Coronavirus disease of 2019 (COVID-19) is a highly contagious respiratory infection that is caused by the severe acute respiratory syndrome coronavirus 2. Although most people are immunocompetent to the virus, a small group fail to mount an effective antiviral response and develop chronic infections that trigger hyperinflammation. This results in major complications, including acute respiratory distress syndrome, disseminated intravascular coagulation, and multiorgan failure, which all carry poor prognoses. Emerging evidence suggests that the complement system plays a key role in this inflammatory reaction. Indeed, patients with severe COVID-19 show prominent complement activation in their lung, skin, and sera, and those individuals who were treated with complement inhibitors all recovered with no adverse reactions. These and other studies hint at complement's therapeutic potential in these sequalae, and thus, to support drug development, in this review, we provide a summary of COVID-19 and review complement's role in COVID-19 acute respiratory distress syndrome and coagulopathy.

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Section: Covid-19 Immunophenotypesmentioning

confidence: 99%

COVID-19: Complement, Coagulation, and Collateral Damage

Kemper

Woodruff

2020

The Journal of Immunology

147

139

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“…An increased NK group 2 member A (NKG2A) expression as a heterodimeric inhibitory receptor can also result in functional exhaustion of NK cells in patients with SARS-CoV-2 infection. Indeed, the total number of NK cells declines during the COVID-19 and the number of NK cells is simultaneously increased with the reduced expression of NKG2A after recovery (Yaqinuddin and Kashir, 2020;Qin et al, 2020), while this is associated with significantly decreased expression of the activation markers including CD107a, IFN-g, IL-2, and TNF-a in T and NK cells of patients with severe COVID-19 (Antonioli et al, 2020;Zheng et al, 2020). In this respect, a study by Vabret et al revealed crosstalk between monocytes and NK cells that results in NK cell recruitment from the peripheral blood to the lungs and killing of SARS-CoV-2-infected cells.…”

Section: Nk Cells-mediated Antiviral Immune Response To Sars-cov2mentioning

confidence: 99%

Harnessing Memory NK Cell to Protect Against COVID-19

Soleimanian

Yaghobi

2020

Front. Pharmacol.

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The worldwide struggle against the coronavirus disease 2019 (COVID-19) as a public health crisis continues to sweep across the globe. Up to now, effective antiviral treatment against COVID-19 is not available. Therefore, throughout virus infections, a thorough clarification of the virus-host immune system interactions will be most probably helpful to encounter these challenges. Emerging evidence suggests that just like SARS and MERS, COVID-19 primarily suppresses the innate immune system, enabling its stable propagation during the early stage of infection. Consequently, proinflammatory cytokines and chemokines have been increasing during infection progression associated with severe lung pathology. It is imperative to consider hyper inflammation in vaccine designing, as vaccine-induced immune responses must have a protective role against infection without leading to immunopathology. Among the front-line responders to viral infections, Natural Killer (NK) cells have immense therapeutic potential, forming a bridge between innate and adaptive responses. A subset of NK cells exhibits putatively increased effector functions against viruses following pathogen-specific and immunization. Memory NK cells have higher cytotoxicity and effector activity, compared with the conventional NK cells. As a pioneering strategy, prompt accumulation and long-term maintenance of these memory NK cells could be an efficacious viral treatment. According to the high prevalence of human cytomegalovirus (HCMV) infection in the world, it remains to be determined whether HCMV adaptive NK cells could play a protective role against this new emerging virus. In addition, the new adaptive-like KIR+NKG2C+ NK cell subset (the adaptivelike lung tissue residue [tr]NK cell) in the context of the respiratory infection at this site could specifically exhibit the expansion upon COVID-19. Another aspect of NK cells we should note, utilizing modified NK cells such as allogeneic off-the-shelf CAR-NK cells as a state-of-the-art strategy for the treatment of COVID-19. In this line, we speculate introducing NKG2C into chimeric antigen receptors in NK cells might be a potential approach in future viral immunotherapy for emerging viruses. In this contribution, we will briefly discuss the current status and future perspective of NK cells, which provide to successfully exploit NK cellmediated antiviral activity that may offer important new tools in COVID-19 treatment.

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“…The NK cells depletion was inversely correlated with increase in expression of Natural Killer Cell Receptors (NKG2A) (39). The same has been observed in COVID-19 patients where NKG2A expression was up-regulated (40). Therefore, the available evidences suggest that the tea polyphenols down regulating NKG2A to induce NK cells can play an important role in early stages of virus infection.…”

Section: Tea Polyphenols and Alkaloids Role In Innate Immunitymentioning

confidence: 65%

Tea Bioactive Modulate Innate Immunity: In Perception to COVID-19 Pandemic

Chowdhury

Barooah

2020

Front. Immunol.

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Innate immunity impairment led to disruption in cascade of signaling pathways upregulating pro-inflammatory cytokines, diminish interferons, depleted natural killer cells and activate reactive oxygen species production. These conditions severely affected body's ability to fight against infectious diseases and also plays a pivotal role in disease progression. Here, in emphasis is on nutritional immunity for regulating effective innate immune response for combating against infectious diseases like novel coronavirus disease (COVID 19). Drawing from discoveries on in-vitro experiments, animal models and human trials, tea polyphenols, micronutrients, and vitamins has the potential to modulate and enhance innate immune response. This article provides a comprehensive review on tea (Camellia sinensis L) infusion (a hot water extract of dried processed tea leaves prepared from young shoots of tea plant) as an innate immunity modulator. Tea infusion is rich in polyphenols; epigallocatechin gallate (EGCG) and theaflavin (TF), major green and black tea polyphenols, respectively. Studies showed their immunomodulatory competence. Tea infusions are also rich in alkaloids; caffeine and its intermediates, theophylline and theobromine, which have anti-inflammatory properties. Tea plant being an acidophilic perennial crop can accumulate different micronutrients, viz., copper (Cu), iron (Fe), manganese (Mn), selenium (Se), and zinc (Zn) from growing medium, i.e., from soil, which led to their considerable presence in tea infusion. Micronutrients are integral part of innate immune response. Overall, this review presents tea infusion as an important source of nutritional immunity which can enhance innate immune response in order to mitigate the unprecedented COVID-19 pandemic.

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NKG2A and COVID-19: another brick in the wall

Cited by 86 publications

References 24 publications

COVID-19: Complement, Coagulation, and Collateral Damage

COVID-19: Complement, Coagulation, and Collateral Damage

Harnessing Memory NK Cell to Protect Against COVID-19

Tea Bioactive Modulate Innate Immunity: In Perception to COVID-19 Pandemic

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