ArticleJournal of virology1994
Augmentation of pathogenesis of coxsackievirus B3 infections in mice by exogenous administration of interleukin-1 and interleukin-2.
Article in Journal of virology, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
28 citing papers in PubMed, 102 citations in OpenAlex.
- IL-33/ST2 Signaling Protects the Heart by Restraining Inflammation and Parasite Burden duringACS infectious diseases · 2026Article
- Spironolactone alleviates myocardial fibrosis via inhibition of Ets-1 in mice with experimental autoimmune myocarditis.Experimental and therapeutic medicine · 2022Article
- Article
- Induction of a broad spectrum of inflammation-related genes by Coxsackievirus B3 requires Interleukin-1 signaling.Medical microbiology and immunology · 2013Article
- Autoimmunity in Coxsackievirus B3 induced myocarditis: role of estrogen in suppressing autoimmunity.Future virology · 2010Article
- Tumor necrosis factor-alpha promotes myocarditis in female mice infected with coxsackievirus B3 through upregulation of CD1d on hematopoietic cells.Viral immunology · 2010Article
- Effect of interleukin-15 on the course of myocarditis in Coxsackievirus B3-infected BALB/c mice.The Canadian journal of cardiology · 2009Article
- Diagnosis and management of viral myocarditis.Current treatment options in cardiovascular medicine · 2007Article
- Regulating inflammation in the heart.International journal of biomedical science : IJBS · 2007Article
- Myocardial remodeling in viral heart disease: possible interactions between inflammatory mediators and MMP-TIMP system.Heart failure reviews · 2004Review
- Amyocarditic coxsackievirus B3 causes myocarditis in immunocompromised mice.Experimental and clinical cardiology · 2003Article
- Vgamma4(+) T cells promote autoimmune CD8(+) cytolytic T-lymphocyte activation in coxsackievirus B3-induced myocarditis in mice: role for CD4(+) Th1 cells.Journal of virology · 2002Article
- Gammadelta T cells promote a Th1 response during coxsackievirus B3 infection in vivo: role of Fas and Fas ligand.Journal of virology · 2002Article
- An approach to the treatment of pediatric myocarditis.Paediatric drugs · 2002Review
- Expression of immunoregulatory cytokines by recombinant coxsackievirus B3 variants confers protection against virus-caused myocarditis.Journal of virology · 2001Article
- Cytokines and their receptors in cardiovascular diseases--role of gp130 signalling pathway in cardiac myocyte growth and maintenance.International journal of experimental pathology · 2000Review
- Hormonal regulation of CD4(+) T-cell responses in coxsackievirus B3-induced myocarditis in mice.Journal of virology · 1999Article
- IgG subclass reactivity to human cardiac myosin in cardiomyopathy patients is indicative of a Th1-like autoimmune disease.Clinical and experimental immunology · 1999Article
- [Therapy of dilated cardiomyopathies with and without inflammation].Medizinische Klinik (Munich, Germany : 1983) · 1998Review
- Innovative drug treatments for viral and autoimmune myocarditis.Journal of clinical pharmacology · 1998Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Two variants of coxsackievirus B3 (CVB3) which differ dramatically in the ability to induce myocarditis in BALB/c mice were studied. H3 virus infection of murine monocytes in vitro resulted in release of concentrations of interleukin 1 (IL-1) and alpha/beta interferon that were high compared with those of cells infected with the H310A1 virus variant. In vivo, H3 virus infection caused substantial inflammatory cell infiltration of the myocardium, and lymphocytes from these animals gave predominantly Th1-cell responses to either whole H3 virus or overlapping peptides of the CVB3 vp1 capsid protein, as determined by IL-2 production. In contrast, H310A1 virus infection produced minimal myocarditis and Th1-cell responses, but Th2-cell activation was more pronounced than in H3 virus-infected mice (as determined by IL-4 concentrations). Exogenous treatment of H310A1 virus-infected mice with either IL-1 or IL-2 restored both myocarditis susceptibility and Th1-cell responses to whole virus and vp1 peptides. Furthermore, H310A1 virus-infected mice given exogenous IL-1 showed substantial in situ IL-2 deposition in the myocardium. These results indicate that CVB3-induced myocarditis may depend upon release of specific cytokines during infection and that activation of Th1 cells may be an important factor in pathogenesis.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.