Genetics of Susceptibility to Viral Myocarditis in Mice

Rose, Noel R.; Neumann, David; Herskowitz, Ahvie; Traystman, Monica D.; Beisel, Kirk W.

doi:10.1159/000157122

Cited by 40 publications

(22 citation statements)

References 22 publications

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“…Susceptibility to EAM varies among different strains of mice and is influenced by both MHC and non-MHC genes (24,25). However, unlike most models of autoimmune disease, non-MHC genes seem to have the greatest influence in EAM.…”

Section: Discussionmentioning

confidence: 99%

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Two Autoimmune Diabetes Loci Influencing T Cell Apoptosis Control Susceptibility to Experimental Autoimmune Myocarditis

Güler

Ligons

Wang

et al. 2005

The Journal of Immunology

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The pathogenesis of immune-mediated myocarditis depends on genetic and environmental factors. To study the genetic mechanisms, we have developed a model of experimental autoimmune myocarditis in the A.SW mouse. Here we provide evidence that loci on murine chromosome 6, and possibly chromosome 1, are involved in regulating susceptibility. Moreover, these loci overlap with loci implicated in other autoimmune diseases including diabetes in the NOD mouse. These two loci also regulate apoptosis in thymocytes as well as peripheral T cells in the NOD mouse, and we report further that A.SW mice demonstrate the same characteristics in apoptosis. These results suggest that common pathogenetic mechanisms involving apoptosis of both thymic and peripheral T cells are shared by multiple autoimmune diseases.

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Section: Discussionmentioning

confidence: 99%

“…We initially observed that this trait was influenced by the H-2 locus but that non-H-2 background genes play a dominant role (24,25). To focus on non-H-2 loci, we fixed the H-2 locus and compared susceptibility to cardiac myosin-induced EAM in the H-2 s congenic strains A.SW and B10.S.…”

Section: Susceptibility To Eam Is a Quantitative Heritable Traitmentioning

confidence: 99%

Two Autoimmune Diabetes Loci Influencing T Cell Apoptosis Control Susceptibility to Experimental Autoimmune Myocarditis

Güler

Ligons

Wang

et al. 2005

The Journal of Immunology

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“…However, not all individuals infected with a specific pathogen will develop myocarditis. Clearly, the genetic composition of the host is important in determining disease susceptibility (6,7). At least part of this genetic susceptibility is determined by the type of immune response generated by the host.…”

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confidence: 99%

Vγ1+ T Cells Suppress and Vγ4+ T Cells Promote Susceptibility to Coxsackievirus B3-Induced Myocarditis in Mice

Huber

Graveline

Newell

et al. 2000

The Journal of Immunology

137

124

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Coxsackievirus B3 infections of C57BL/6 mice, which express the MHC class II IA but not IE Ag, results in virus replication in the heart but minimal myocarditis. In contrast, Bl.Tg.Eα mice, which are C57BL/6 mice transgenically induced to express IE Ag, develop significant myocarditis upon Coxsackievirus B3 infection. Despite this difference in inflammatory damage, cardiac virus titers are similar between C57BL/6 and Bl.Tg.Eα mice. Removing γδ T cells from either strain by genetic manipulation (γδ knockout(ko)) changes the disease phenotype. C57BL/6 γδ ko mice show increased myocarditis. In contrast, Bl.Tg.Eα γδ ko mice show decreased cardiac inflammation. Flow cytometry revealed a difference in the γδ cell subsets in the two strains, with Vγ1 dominating in C57BL/6 mice, and Vγ4 predominating Bl.Tg.Eα mice. This suggests that these two Vγ-defined subsets might have different functions. To test this possibility, we used mAb injection to deplete each subset. Mice depleted of Vγ1 cells showed enhanced myocarditis, whereas those depleted of Vγ4 cells suppressed myocarditis. Adoptively transfusing enriched Vγ4+ cells to the C57BL/6 and Bl.Tg.Eα γδ ko strains confirmed that the Vγ4 subset promoted myocarditis. Th subset analysis suggests that Vγ1+ cells biased the CD4+ T cells to a dominant Th2 cell response, whereas Vγ4+ cells biased CD4+ T cells toward a dominant Th1 cell response.

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“…The closely related CVB, as the best-studied non-PV enterovirus group, represents an attractive enterovirus system with which to complement or replace chimeric PV vaccine development. Because of the high etiologic association of the CVB and Ad2 with human viral myocarditis (4,21,30,40,53,56,57,62,66, 67), we tested whether an artificially attenuated strain of CVB3 could express an antigenic sequence of Ad2 and then whether the progeny virus could induce protective immunity against both viruses in an experimental mouse system. The data presented in this report demonstrate that a CVB can be engineered to express an antigenic polypeptide from within the CVB3 ORF and that the resulting virus induces both neutralizing and binding antibodies against Ad2 and CVB3.…”

Section: Vol 74 2000 Ad Epitope Expression In Group B Coxsackievirumentioning

confidence: 99%

Expression of an Antigenic Adenovirus Epitope in a Group B Coxsackievirus

Höfling

Tracy

Chapman

et al. 2000

J Virol

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Genetics of Susceptibility to Viral Myocarditis in Mice

Cited by 40 publications

References 22 publications

Two Autoimmune Diabetes Loci Influencing T Cell Apoptosis Control Susceptibility to Experimental Autoimmune Myocarditis

Two Autoimmune Diabetes Loci Influencing T Cell Apoptosis Control Susceptibility to Experimental Autoimmune Myocarditis

Vγ1+ T Cells Suppress and Vγ4+ T Cells Promote Susceptibility to Coxsackievirus B3-Induced Myocarditis in Mice

Expression of an Antigenic Adenovirus Epitope in a Group B Coxsackievirus

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