Natural killer cell activation after infection with lactate dehydrogenase-elevating virus

Markine-Goriaynoff, Dominique; Hulhoven, Xavier; Cambiaso, Cesar; Monteyne, Philippe; Briet, Thérèse; Gonzalez, Maria-Dolores; Coulie, Pierre G.; Coutelier, Jean‐Paul

doi:10.1099/0022-1317-83-11-2709

Cited by 33 publications

(46 citation statements)

References 42 publications

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“…Interestingly, no major modification in the cellular origin of IFN-c was found in animals deficient for type I IFN receptor (Table 1). The preponderant role of NK cells in IFN-c production following LDV infection fits well with previous observations suggesting the involvement of this cell population in this process (Markine-Goriaynoff et al, 2002).…”

supporting

confidence: 77%

“…Cell populations were determined by using a fluoresceinated anti-mouse DX5 monoclonal antibody (mAb) (BD Biosciences) as described previously (Markine-Goriaynoff et al, 2002). Production of IFN-c by these cells was analysed by using a mouse IFN-c secretion assay detection kit following the manufacturer's instructions (Miltenyi Biotec).…”

mentioning

confidence: 99%

“…Because type I IFNs may modulate the replication of viruses dramatically, with possible consequences on the subsequent immune response, LDV viraemia was measured in 129/Sv and IFNAR KO mice by a sensitive particlecounting immunoassay based on the agglutination of latex beads coated with two different anti-LDV mAbs by viral particles, as described previously (Markine-Goriaynoff et al, 2002). A mere 2-fold increase in LDV titres, which was, however, significant (P50.0022 by non-parametric Mann-Whitney test), was observed in mice unresponsive to type I IFNs at 16 h post-infection, which corresponds to the highest level of viraemia (Coutelier & Brinton, 2007), as shown in Fig.…”

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confidence: 99%

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Distinct gamma interferon-production pathways in mice infected with lactate dehydrogenase-elevating virus

Le-Thi-Phuong

Thirion

Coutelier

2007

Journal of General Virology

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Two distinct pathways of gamma interferon (IFN-γ) production have been found in mice infected with lactate dehydrogenase-elevating virus. Both pathways involve natural killer cells. The first is mostly interleukin-12-independent and is not controlled by type I interferons. The second, which is suppressed by type I interferons, leads to increased levels of IFN-γ production and requires the secretion of interleukin-12. This regulation of IFN-γ production by type I interferons may help to control indirect pathogenesis induced by this cytokine.

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confidence: 77%

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confidence: 99%

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confidence: 99%

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Distinct gamma interferon-production pathways in mice infected with lactate dehydrogenase-elevating virus

Le-Thi-Phuong

Thirion

Coutelier

2007

Journal of General Virology

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“…Indeed, IFN-␥ production after LDV infection reaches a peak 18 hours after virus inoculation, and then rapidly decreases. 16 In addition to IFN-␥, we cannot exclude that other cytokines, including interleukins 2 and 12 and macrophage colony-stimulating factor (M-CSF) may also be involved in this virally induced activation of macrophage functions. For personal use only.…”

Section: Discussionmentioning

confidence: 99%

“…Because macrophage functions, and especially phagocytosis, are enhanced by IFN-␥, a cytokine produced in the course of LDV infection, 16 this cytokine was suspected as a mediator of LDVinduced enhancement of antiplatelet antibody pathogenicity. The causative role of IFN-␥ was shown in mice genetically unable to respond to this cytokine.…”

Section: Discussionmentioning

confidence: 99%

Exacerbation of autoantibody-mediated thrombocytopenic purpura by infection with mouse viruses

Musaji

Cormont

Thirion

et al. 2004

Blood

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Antigenic mimicry has been proposed as a major mechanism by which viruses could trigger the development of immune thrombocytopenic purpura (ITP). However, because antigenic mimicry implies epitope similarities between viral and self antigens, it is difficult to understand how widely different viruses can be involved by this sole mechanism in the pathogenesis of ITP. Here, we report that in mice treated with antiplatelet antibodies at a dose insufficient to induce clinical disease by themselves, infection with lactate dehydrogenase-elevating virus (LDV) was followed by severe thrombocytopenia and by the appearance of petechiae similar to those observed in patients with ITP. A similar exacerbation of antiplateletmediated thrombocytopenia was induced by mouse hepatitis virus. This enhancement of antiplatelet antibody pathogenicity by LDV was not observed with F(ab) 2 fragments, suggesting that phagocytosis was involved in platelet destruction. Treatment of mice with clodronate-containing liposomes and with total immunoglobulin G (IgG) indicated that platelets were cleared by macrophages. The increase of thrombocytopenia triggered by LDV after administration of antiplatelet antibodies was largely suppressed in animals deficient for ␥-interferon receptor. Together, these results suggest that viruses may exacerbate autoantibody-mediated ITP by activating macrophages through ␥-interferon production, a mechanism that may account for the pathogenic similarities of multiple infectious agents. (Blood. 2004;

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Mouse

Percy¹,

Barthold

2007

Pathology of Laboratory Rodents and Rabbits

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The laboratory mouse is an artificial creation, and there is no true "wildtype" laboratory mouse. Furthermore, there is no such thing as "normal" microflora, since laboratory mice are maintained in microbially pristine environments devoid of pathogens and opportunistic pathogens, as well as other commensal flora/fauna. House mice, from which laboratory mice originated, are represented by several species and subspecies native to the Old World. Laboratory mice are largely derived from domesticated "fancy mice" that arose from many years of trading of mouse variants among fanciers in Europe, Asia, North America, and Australia. The laboratory mouse genome, including its retroelements, is a mosaic derived from different subspecies of the Mus musculus complex, including M.m. domesticus, M.m. musculus, M.m. castaneus, M.m. molossinus (a natural hybrid of M.m. musculus and M.m. castaneus), and M. bactrianus.The genome of M.m. domesticus is the predominant contributor to most strains of mice, but many inbred strains share a common "Eve" with a mitochondrial genome of M.m. musculus origin, and a common "Adam" that contributed their Y chromosome from Asian mice. In addition, there is evidence that other Mus species, outside of the M. musculus complex, may have contributed to the genome of some laboratory mouse strains. The C57BL mouse genome contains a contribution from M. spretus. The 1st inbred mouse (DBA), and other strains with DBA genetic contributions, was partially derived from Japanese waltzing mice with M. bactrianus parentage. Perhaps the only laboratory mouse that is derived from a single species (subspecies), M.m. domesticus, is the "Swiss" mouse, but there is a high likelihood that several Swiss stocks and strains have been genetically corrupted.There are over 450 inbred strains of laboratory mice that have arisen during the last century, and these strains, which were selectively inbred to pan-genomic homozygosity for purposes entirely unrelated to modern research, are the foundation upon which literally thousands of spontaneous mutants and GEMs have been built. Additional inbred strains have been developed from wild mice (M.m. castaneus, M. spretus, etc.). Furthermore, "outbred" mice (mostly Swiss mice) are highly homozygous and nearly inbred. There is no such thing as an outbred laboratory mouse with a fully heterozygous genome representative of wildtype M. musculus, and there is no wild mouse genetic counterpart of the laboratory mouse. When working with mice, the pathologist must also become facile with hybrids,

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Natural killer cell activation after infection with lactate dehydrogenase-elevating virus

Cited by 33 publications

References 42 publications

Distinct gamma interferon-production pathways in mice infected with lactate dehydrogenase-elevating virus

Distinct gamma interferon-production pathways in mice infected with lactate dehydrogenase-elevating virus

Exacerbation of autoantibody-mediated thrombocytopenic purpura by infection with mouse viruses

Mouse

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