ArticleProceedings of the National Academy of Sciences of the United States of America1994
Alterations in major histocompatibility complex association of myocarditis induced by coxsackievirus B3 mutants selected with monoclonal antibodies to group A streptococci.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 43 citations in OpenAlex.
- T-Cell Receptor Sequences Identify Combined Coxsackievirus-International journal of molecular sciences · 2024Article
- Designing a multi-epitope vaccine against coxsackievirus B based on immunoinformatics approaches.Frontiers in immunology · 2022Article
- Immune checkpoint inhibitor-associated myocarditis: manifestations and mechanisms.The Journal of clinical investigation · 2021Review
- Triggers of Inflammatory Heart Disease.Frontiers in cell and developmental biology · 2020Review
- Molecular Mimicry, Autoimmunity, and Infection: The Cross-Reactive Antigens of Group A Streptococci and their Sequelae.Microbiology spectrum · 2019Review
- miPepBase: A Database of Experimentally Verified Peptides Involved in Molecular Mimicry.Frontiers in microbiology · 2017Article
- Autoimmune myocarditis, valvulitis, and cardiomyopathy.Current protocols in immunology · 2013Article
- The nonideal coiled coil of M protein and its multifarious functions in pathogenesis.Advances in experimental medicine and biology · 2011Review
- Autoimmune disease triggered by infection with alphaproteobacteria.Expert review of clinical immunology · 2009Article
- The role of infections in autoimmune disease.Clinical and experimental immunology · 2009Review
- Roles of tumor necrosis factor alpha (TNF-alpha) and the p55 TNF receptor in CD1d induction and coxsackievirus B3-induced myocarditis.Journal of virology · 2005Article
- Evidence of Borrelia autoimmunity-induced component of Lyme carditis and arthritis.Journal of clinical microbiology · 2005Article
- Induction of myocarditis and valvulitis in lewis rats by different epitopes of cardiac myosin and its implications in rheumatic carditis.The American journal of pathology · 2002Article
- Cardiac myosin and the TH1/TH2 paradigm in autoimmune myocarditis.The American journal of pathology · 2001Review
- Molecular mimicry and immune-mediated diseases.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 1998Review
- A mutation in the puff region of VP2 attenuates the myocarditic phenotype of an infectious cDNA of the Woodruff variant of coxsackievirus B3.Journal of virology · 1996Article
- Modulation of cytokine expression by CD4+ T cells during coxsackievirus B3 infections of BALB/c mice initiated by cells expressing the gamma delta + T-cell receptor.Journal of virology · 1996Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Three monoclonal antibodies (mAbs), 49.8.9, 36.2.2, and 54.2.8, made to the group A streptococcus M5 serotype identify crossreactive epitopes in cardiac tissues and also neutralize a highly myocarditic variant of coxsackievirus B3 (H3). Mutants of H3 were selected with these mAbs and evaluated for pathogenicity compared with the wild-type virus. H3 and the mutant variants selected with mAbs 36.2.2 (H3-36) and 54.2.8 (H3-54) induced severe myocarditis in DBA/2 (H-2d) and A/J (H-2a) male mice, whereas CBA (H-2k) mice were disease resistant. The virus variant isolated with mAb 49.8.9 (H3-49) was strikingly different and caused disease in CBA and A/J mice but not in DBA/2 animals, suggesting that the major histocompatibility complex association of the disease had been altered. This hypothesis was confirmed by using B10 congenic mice. In addition, T lymphocytes from the H3 and H3-49 virus-infected mice responded to distinctly different peptides in the streptococcal M protein, suggesting that certain epitopes of infectious agents which are shared with host tissues may be critical in determining disease susceptibility in genetically distinct individuals.
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Registered trials
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.