Mouse Parvovirus Infection Potentiates Allogeneic Skin Graft Rejection and Induces Syngeneic Graft Rejection1

McKisic, M D; Macy, James D; Delano, Margaret L.; Jacoby, Robert O.; Paturzo, Frank X.; Smith, Abigail L.

doi:10.1097/00007890-199806150-00005

Cited by 36 publications

(27 citation statements)

References 52 publications

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“…In a related study of BALB/c mice experimentally infected with MPV1a, infected mice had increased rejection of both allogeneic and syngeneic skin grafts, but the allogeneic-reactive T cells had decreased proliferative capacity. 85 No subsequent reports have corroborated these findings with any culture adapted or field strain of MPV. At this time, no long-term immunological effects have been shown for natural infection of mice with any field strain of MVM.…”

Section: Viral Agentsmentioning

confidence: 91%

“…Two studies in the 1990s found altered immune function in mice experimentally infected with MPV1a, a culture-adapted strain discovered because of its effects on T-lymphocyte cultures. 85,84 In these studies, BALB/ c mice were inoculated with 10 6 TCID intraperitoneally and 10 5 TCID oronasally. Infected mice had accelerated rejection of tumor allografts but decreased killing by T cells.…”

Section: Viral Agentsmentioning

confidence: 99%

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Of Mice and Microflora

et al. 2011

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The phenotype of genetically engineered mice is a combination of both genetic and environmental factors that include the microflora of the mouse. The impact a particular microbe has on a mouse reflects the host-microbe interaction within the context of the mouse genotype and environment. Although often considered a confounding variable, many host-microbe interactions have resulted in the generation of novel model systems and characterization of new microbial agents. Microbes associated with overt disease in mice have been the historical focus of the laboratory animal medical and pathology community and literature. The advent of genetic engineering and the complex of mouse models have revealed previously unknown or disregarded agents that now oblige the attention of the biomedical research community. The purpose of this article is to describe and illustrate how phenotypes can be affected by microflora by focusing on the infectious diseases present in genetically engineered mouse (GEM) colonies of our collective institutions and by reviewing important agents that are rarely seen in most research facilities today. The goal is to introduce the concept of the role of microflora on phenotypes and in translational research using GEM models.

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Section: Viral Agentsmentioning

confidence: 91%

Section: Viral Agentsmentioning

confidence: 99%

Of Mice and Microflora

et al. 2011

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“…Anti-CD4 (GK1.5) and anti-CD8 (2.43) mAb in the form of ascites fluid were administered i.p. to B6-Igh6 KO donor mice, as described (29). Control mice were treated with an irrelevant mAb of the same isotype, D468.3.…”

Section: Figurementioning

confidence: 99%

Cutting Edge: T Cell-Mediated Pathology in Murine Lyme Borreliosis

McKisic

Redmond

Barthold

2000

The Journal of Immunology

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Even in the absence of an appropriate model or direct evidence, T cells have been hypothesized to exacerbate the manifestations of Lyme disease. To define definitely the role of T cells in Lyme disease, the course of disease in immunocompetent and B cell-deficient mice was compared. By 8 wk postinoculation, immunocompetent mice resolved both carditis and arthritis, whereas foci of myocarditis and severe destructive arthritis characterized disease of B cell-deficient mice. Cell transfer experiments using infected B6-Rag1 knock out mice demonstrated that: 1) innate immunity mediated the initial sequelae of infection, 2) transferring both naive T cells and B cells induced resolution of carditis and arthritis, 3) infected mice reconstituted with T cells developed myocarditis and severe destructive arthritis, and 4) CD4+ T cells were responsible for the observed immune-mediated pathology. These data demonstrate directly the deleterious effect of T cells in Lyme disease.

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“…For instance, BALB/c mice, infected by the B19 peptide, develop a strong anti-B19 parvovirus response and autoantibody activity against keratin, collagen II, cardiolipin, and single-stranded DNA. 49,50 However, the interaction between parvovirus B19 capsid protein and AT 1 receptor is far from understood. Epitope mimicry cannot be excluded and should be investigated further.…”

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confidence: 99%

Prevalence of Agonistic Autoantibodies Against the Angiotensin II Type 1 Receptor and Soluble fms-Like Tyrosine Kinase 1 in a Gestational Age–Matched Case Study

et al. 2009

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Abstract-We showed earlier that activating autoantibodies against the angiotensin II type 1 (AT 1 ) receptor (AT1-AA) circulate in preeclamptic women. They may be involved in the pathogenesis of preeclampsia. Protein alignment suggests that the binding site for AT1-AAs is highly homologous to the capsid protein VP2 of parvovirus B19. We performed a prospective, nested, case-control study of 30 gestational age-matched women with preeclampsia and 30 normotensive pregnant women. We measured AT1-AA, soluble fms-like tyrosine kinase 1 (sFlt-1), and serum immunoglobulin G against parvovirus B19 proteins. AT1-AAs were present in 70% of preeclamptic patients and absent in 80% of controls. Prediction by AT1-AA was improved in late-onset preeclampsia. The discrimination for sFlt-1 was 96%. We did not find an interaction between sFlt-1 and AT1-AA. A human monoclonal immunoglobulin G antibody against parvovirus B19 VP2-protein showed a positive reaction in the AT1-AA bioassay, which could be blocked by an AT 1 receptor blocker, as well as by the epitope amino acid sequence. Immunoglobulin G against parvovirus B19 proteins was similarly distributed between preeclamptic patients and controls and had no significant importance. We detected significantly more AT1-AA in women with an immune response corresponding with parvovirus B19 infection corresponding with a distant viral infection associated with virus elimination. We concluded that AT1-AAs were common in patients with preeclampsia in a prospective case-control study, although sFlt-1 was a superior biomarker. AT1-AA may represent a better marker for late disease, whereas sFlt1 is a better marker for early onset disease. Key Words: preeclampsia Ⅲ activating autoantibodies Ⅲ angiogenesis Ⅲ parvovirus B19 Ⅲ molecular mimicry P reeclampsia is defined as new-onset hypertension after 20 weeks' gestation accompanied by new-onset proteinuria; the condition causes acute morbidity and mortality. 1,2 The incidence is 2% to 5% worldwide and is associated with subsequent cardiovascular diseases in both mother and child. 3 The pathogenesis is unknown but is likely to be multifactorial. 4 We described circulating autoantibodies directed at the second extracellular loop of the angiotensin (Ang) II type 1 (AT 1 ) receptor (AT1-AA) in women with preeclampsia. 5 AT1-AAs induce reactive oxygen species, inhibit trophoblast migration, and occur in rat models. 6 -8 AT1-AAs induced preeclampsia-like symptoms in C57BL/6J mice by passive transfer. 9 However, AT1-AAs are not specific for preeclampsia and also occur in patients with humoral kidney transplant rejection. 10 An epitope on the second extracellular loop of the human AT 1 receptor (AFHYESQ) represents the binding site for AT1-AAs; the same sequence inhibits the AT1-AAmediated effects completely in vivo and in vitro. The epitope is highly homologous to the capsid protein VP2 from parvovirus B19 (AFHYETQ).Parvovirus B19 is a single-stranded DNA virus and can cause erythema infectiosum, a generally (but not always) mild childhood exanthem. 11,...

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Mouse Parvovirus Infection Potentiates Allogeneic Skin Graft Rejection and Induces Syngeneic Graft Rejection1

Abstract: These results suggest that MPV-1 infection of skin-grafted mice may disrupt normal mechanisms of peripheral tolerance and provide a unique model to study virus-induced autoimmunity.

Cited by 36 publications

References 52 publications

Of Mice and Microflora

Of Mice and Microflora

Cutting Edge: T Cell-Mediated Pathology in Murine Lyme Borreliosis

Prevalence of Agonistic Autoantibodies Against the Angiotensin II Type 1 Receptor and Soluble fms-Like Tyrosine Kinase 1 in a Gestational Age–Matched Case Study

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