Production of protective gamma interferon by natural killer cells during early mouse hepatitis virus infection

Thirion, Gaëtan; Coutelier, Jean‐Paul

doi:10.1099/vir.0.005876-0

Cited by 7 publications

(6 citation statements)

References 30 publications

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“…The finding that IFN-γ-mediated transcriptional responses are not dramatically affected in the absence of type I IFN signalling is in agreement with reports referred to above and with a recent publication by Ireland et al [18], which shows that IFN-γ expression is significantly induced in the CNS of MHV-infected IFNAR-/-mice. While the production of IFN-γ by NK cells plays a major role in the protection against infection with MHV [43][44][45][46][47], the IFN-γ-mediated transcriptional responses that we observed were not protective against acute MHV infection in the IFNAR-/-mice.…”

Section: Induction Of Gene Expression Correlates With the Viral Loadmentioning

confidence: 90%

Type I interferon receptor-independent and -dependent host transcriptional responses to mouse hepatitis coronavirus infection in vivo

et al. 2009

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BackgroundThe role of type I IFNs in protecting against coronavirus (CoV) infections is not fully understood. While CoVs are poor inducers of type I IFNs in tissue culture, several studies have demonstrated the importance of the type I IFN response in controlling MHV infection in animals. The protective effectors against MHV infection are, however, still unknown.ResultsIn order to get more insight into the antiviral gene expression induced in the brains of MHV-infected mice, we performed whole-genome expression profiling. Three different mouse strains, differing in their susceptibility to infection with MHV, were used. In BALB/c mice, which display high viral loads but are able to control the infection, 57 and 121 genes were significantly differentially expressed (≥ 1.5 fold change) upon infection at 2 and 5 days post infection, respectively. Functional association network analyses demonstrated a strong type I IFN response, with Irf1 and Irf7 as the central players. At 5 days post infection, a type II IFN response also becomes apparent. Both the type I and II IFN response, which were more pronounced in mice with a higher viral load, were not observed in 129SvEv mice, which are much less susceptible to infection with MHV. 129SvEv mice lacking the type I interferon receptor (IFNAR-/-), however, were not able to control the infection. Gene expression profiling of these mice identified type I IFN-independent responses to infection, with IFN-γ as the central player. As the BALB/c and the IFNAR-/- 129SvEv mice demonstrated very similar viral loads in their brains, we also compared their gene expression profiles upon infection with MHV in order to identify type I IFN-dependent transcriptional responses. Many known IFN-inducible genes were detected, several of which have previously been shown to play an important protective role against virus infections. We speculate that the additional type I IFN-dependent genes that we discovered may also be important for protection against MHV infection.ConclusionTranscriptional profiling of mice infected with MHV demonstrated the induction of a robust IFN response, which correlated with the viral load. Profiling of IFNAR-/- mice allowed us to identify type I IFN-independent and -dependent responses. Overall, this study broadens our present knowledge of the type I and II IFN-mediated effector responses during CoV infection in vivo.

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Section: Induction Of Gene Expression Correlates With the Viral Loadmentioning

confidence: 90%

Type I interferon receptor-independent and -dependent host transcriptional responses to mouse hepatitis coronavirus infection in vivo

et al. 2009

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“…F3 rat anti-mouse IFN-γ monoclonal antibody (mAb) [23], purified with protein G-sepharose beads, was injected i.p. into mice at a dose of 500 μg 1 day before and 5 days after LDV infection.…”

Section: Antibodies and Nk Cell Depletionmentioning

confidence: 99%

Lactate dehydrogenase-elevating virus enhances natural killer cell-mediated immunosurveillance of mouse mesothelioma development

Mandour¹,

Soe²,

Uyttenhove³

et al. 2020

Infect Agents Cancer

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Background: Viral infections can reduce early cancer development through enhancement of cancer immunosurveillance. This study was performed to analyse this effect of viral infection in a mouse model of solid tumor. Methods: The experimental model used was the effect of BALB/c mouse infection by lactate dehydrogenaseelevating virus on AB1 mesothelioma cancer development. Results: Acute infection with lactate dehydrogenase-elevating virus strongly reduced in vivo early AB1 mesothelioma growth and death resulting from cancer development. This effect was not due to a direct cytolytic effect of the virus on AB1 cells, but to an in vivo activation of natural killer cells. Gamma-interferon production rather than cytotoxic activity against AB1 cells mediated this protective effect. This gamma-interferon production by natural killer cells was dependent on interleukin-12 production. Conclusions: Together with other reported effects of infectious agents on cancer development, this observation may support the hypothesis that enhancement of innate immunosurveillance against tumors may result from infection with common infectious agents through modulation of the host immune microenvironment.

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“…Viral infections are known to trigger the secretion of several IFN types, including IFN-γ, which is secreted by NK cells after LDV and MHV infection [5,20] and which mediates most observed macrophage activation. Thus, IFN-γ plays a major role in the exacerbation of antibody-mediated thrombocytopenia and anemia induced by viruses, such as LDV [2][3][4]21], as well as in enhanced sensibility to endotoxin shock [22].…”

Section: Discussionmentioning

confidence: 99%

Involvement of Virus-Induced Interferon Production in IgG Autoantibody-Mediated Anemia

Legrain

Gaignage

et al. 2021

IJMS

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Infection with viruses, such as the lactate dehydrogenase-elevating virus (LDV), is known to trigger the onset of autoimmune anemia through the enhancement of the phagocytosis of autoantibody-opsonized erythrocytes by activated macrophages. Type I interferon receptor-deficient mice show enhanced anemia, which suggests a protective effect of these cytokines, partly through the control of type II interferon production. The development of anemia requires the expression of Fcγ receptors (FcγR) I, III, and IV. Whereas LDV infection decreases FcγR III expression, it enhances FcγR I and IV expression in wild-type animals. The LDV-associated increase in the expression of FcγR I and IV is largely reduced in type I interferon receptor-deficient mice, through both type II interferon-dependent and -independent mechanisms. Thus, the regulation of the expression of FcγR I and IV, but not III, by interferons may partly explain the exacerbating effect of LDV infection on anemia that results from the enhanced phagocytosis of IgG autoantibody-opsonized erythrocytes.

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Production of protective gamma interferon by natural killer cells during early mouse hepatitis virus infection

Cited by 7 publications

References 30 publications

Type I interferon receptor-independent and -dependent host transcriptional responses to mouse hepatitis coronavirus infection in vivo

Type I interferon receptor-independent and -dependent host transcriptional responses to mouse hepatitis coronavirus infection in vivo

Lactate dehydrogenase-elevating virus enhances natural killer cell-mediated immunosurveillance of mouse mesothelioma development

Involvement of Virus-Induced Interferon Production in IgG Autoantibody-Mediated Anemia

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