The role of NK cells in fighting the virus infection and sepsis

Ma, Lu; Li, Qi; Cai, Suna; Peng, Hourong; Huyan, Ting; Yang, Hui

doi:10.7150/ijms.59898

Cited by 29 publications

(23 citation statements)

References 188 publications

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“…This difference may be the reason for a more profound deficiency in functional NK cells in NSG mice compared to the NOD strain. An increased activation of and a suggested alleviating effect on the early stage of viral infections by NK cells has been shown for various viral infections such as dengue virus, Zika virus, hantavirus or tick-borne encephalitis virus [84]. While their role in systemic RVFV infection remains unclear in detail, a rise of NK cells in liver and lymph nodes of RVFV-infected mice has been observed previously [44].…”

Section: Discussionmentioning

confidence: 85%

NSG-Mice Reveal the Importance of a Functional Innate and Adaptive Immune Response to Overcome RVFV Infection

Michaely

Rissmann

Keller

et al. 2022

Viruses

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Rift Valley fever (RVF) is a zoonotic disease caused by RVF Phlebovirus (RVFV). The RVFV MP-12 vaccine strain is known to exhibit residual virulence in the case of a deficient interferon type 1 response. The hypothesis of this study is that virus replication and severity of lesions induced by the MP-12 strain in immunocompromised mice depend on the specific function of the disturbed pathway. Therefore, 10 strains of mice with deficient innate immunity (B6-IFNARtmAgt, C.129S7(B6)-Ifngtm1Ts/J, B6-TLR3tm1Flv, B6-TLR7tm1Aki, NOD/ShiLtJ), helper T-cell- (CD4tm1Mak), cytotoxic T-cell- (CD8atm1Mak), B-cell- (Igh-Jtm1DhuN?+N2), combined T- and B-cell- (NU/J) and combined T-, B-, natural killer (NK) cell- and macrophage-mediated immunity (NOD.Cg-PrkdcscidIl2rgtm1WjI/SzJ (NSG) mice) were subcutaneously infected with RVFV MP-12. B6-IFNARtmAgt mice were the only strain to develop fatal disease due to RVFV-induced severe hepatocellular necrosis and apoptosis. Notably, no clinical disease and only mild multifocal hepatocellular necrosis and apoptosis were observed in NSG mice, while immunohistochemistry detected the RVFV antigen in the liver and the brain. No or low virus expression and no lesions were observed in the other mouse strains. Conclusively, the interferon type 1 response is essential for early control of RVFV replication and disease, whereas functional NK cells, macrophages and lymphocytes are essential for virus clearance.

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Section: Discussionmentioning

confidence: 85%

NSG-Mice Reveal the Importance of a Functional Innate and Adaptive Immune Response to Overcome RVFV Infection

Michaely

Rissmann

Keller

et al. 2022

Viruses

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“…These cells express different types of Pattern-recognition receptors (PRRs) to recognize DAMPs and PAMPs (Li and Wu, 2021). In COVID-19 patients, NK cells can kill virus-infected cells by releasing cytotoxic granules or through participating in antibody-dependent cellular cytotoxicity and producing different cytokines and chemokines (Ma et al, 2021).…”

Section: Covid-19 Infection and The Immune System Responsesmentioning

confidence: 99%

Cancer Occurrence as the Upcoming Complications of COVID-19

Rahimmanesh

Shariati

Dana

et al. 2022

Front. Mol. Biosci.

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Previous studies suggested that patients with comorbidities including cancer had a higher risk of mortality or developing more severe forms of COVID-19. The interaction of cancer and COVID-19 is unrecognized and potential long-term effects of COVID-19 on cancer outcome remain to be explored. Furthermore, whether COVID‐19 increases the risk of cancer in those without previous history of malignancies, has not yet been studied. Cancer progression, recurrence and metastasis depend on the complex interaction between the tumor and the host inflammatory response. Extreme proinflammatory cytokine release (cytokine storm) and multi‐organ failure are hallmarks of severe COVID‐19. Besides impaired T-Cell response, elevated levels of cytokines, growth factors and also chemokines in the plasma of patients in the acute phase of COVID-19 as well as tissue damage and chronic low‐grade inflammation in “long COVID‐19” syndrome may facilitate cancer progression and recurrence. Following a systemic inflammatory response syndrome, some counterbalancing compensatory anti-inflammatory mechanisms will be activated to restore immune homeostasis. On the other hand, there remains the possibility of the integration of SARS- CoV-2 into the host genome, which potentially may cause cancer. These mechanisms have also been shown to be implicated in both tumorigenesis and metastasis. In this review, we are going to focus on potential mechanisms and the molecular interplay, which connect COVID-19, inflammation, and immune-mediated tumor progression that may propose a framework to understand the possible role of COVID-19 infection in tumorgenesis and cancer progression.

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“…Our data support a model in which C15 protects infected cells by interfering with engagement of target cells and subsequent activating/inhibitory receptor-based activation of NK cell cytolysis. We eliminated NKG2D (an activating receptor important to NK control of ECTV and a wellstudied viral target (Ma et al, 2016(Ma et al, , 2021)) as the mechanism (Fig. S3 A), but there are many other activating and inhibitory NK cell receptors that C15 could target.…”

Section: C15 Inhibits Nk Cell Contacts With Virus-infected Cellsmentioning

confidence: 99%

The ectromelia virus virulence factor C15 facilitates early viral spread by inhibiting NK cell-infected cell contacts

Peauroi

Carro

Pei

et al. 2022

Preprint

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The success of poxviruses as pathogens depends upon their antagonism of host responses by multiple immunomodulatory proteins. The largest of these expressed by ectromelia virus (the agent of mousepox) is C15, one member of a well-conserved poxviral family previously shown to inhibit T cell activation. Here, we demonstrate by quantitative immunofluorescence imaging that C15 also limits contact between natural killer (NK) cells and infected cells in vivo. This corresponds to an inhibition in the number of total and degranulating NK cells, ex vivo and in vitro, with no detectable impact on NK cell cytokine production nor the transcription of factors related to NK cell recruitment or activation. Thus, in addition to its previously identified capacity to antagonize CD4 T cell activation, C15 inhibits NK cell cytolytic function, which results in increased viral replication and dissemination in vivo. This work builds on a body of literature demonstrating the importance of early restriction of virus within the draining lymph node.

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The role of NK cells in fighting the virus infection and sepsis

Cited by 29 publications

References 188 publications

NSG-Mice Reveal the Importance of a Functional Innate and Adaptive Immune Response to Overcome RVFV Infection

NSG-Mice Reveal the Importance of a Functional Innate and Adaptive Immune Response to Overcome RVFV Infection

Cancer Occurrence as the Upcoming Complications of COVID-19

The ectromelia virus virulence factor C15 facilitates early viral spread by inhibiting NK cell-infected cell contacts

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