| pubmed-article:3004227 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:3004227 | lifeskim:mentions | umls-concept:C0010247 | lld:lifeskim |
| pubmed-article:3004227 | lifeskim:mentions | umls-concept:C0027059 | lld:lifeskim |
| pubmed-article:3004227 | lifeskim:mentions | umls-concept:C0020792 | lld:lifeskim |
| pubmed-article:3004227 | lifeskim:mentions | umls-concept:C0025919 | lld:lifeskim |
| pubmed-article:3004227 | lifeskim:mentions | umls-concept:C1511649 | lld:lifeskim |
| pubmed-article:3004227 | lifeskim:mentions | umls-concept:C0450254 | lld:lifeskim |
| pubmed-article:3004227 | lifeskim:mentions | umls-concept:C0441712 | lld:lifeskim |
| pubmed-article:3004227 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:3004227 | pubmed:dateCreated | 1986-3-17 | lld:pubmed |
| pubmed-article:3004227 | pubmed:abstractText | DBA/2 and Balb/c mice, both H-2d, develop myocardial inflammation and necrosis when infected with a heart-adapted strain of coxsackievirus Group B, Type 3. Similar inoculation of C57Bl/6 (H-2b) animals results in minimal myocarditis despite equivalent heart virus titers in the three stains. Thus, the host's genetic constitution influences the pathogenesis of the infection. Anti-mouse thymocyte serum and monoclonal Iad antibody effectively prevent myocarditis induction in DBA/2 and Balb/c mice, which demonstrates the importance of the immune system in this disease. Cytolytic T lymphocytes lysing virus-infected and uninfected myocytes and heart-reactive autoantibodies occur in both myocarditis-susceptible strains. Cellular immunity causes the myocardial injury in Balb/c mice. Complement depletion of Balb/c mice using cobra venom factor fails to alter the disease. Similar treatment of DBA/2 animals abrogates inflammation and necrosis, which suggests that heart-reactive antibodies in this strain are primarily responsible for initiating myocardial damage. | lld:pubmed |
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| pubmed-article:3004227 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:3004227 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:3004227 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:3004227 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:3004227 | pubmed:issn | 0002-9440 | lld:pubmed |
| pubmed-article:3004227 | pubmed:author | pubmed-author:HuberS ASA | lld:pubmed |
| pubmed-article:3004227 | pubmed:author | pubmed-author:LodgeP APA | lld:pubmed |
| pubmed-article:3004227 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:3004227 | pubmed:volume | 122 | lld:pubmed |
| pubmed-article:3004227 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:3004227 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:3004227 | pubmed:pagination | 284-91 | lld:pubmed |
| pubmed-article:3004227 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:3004227 | pubmed:year | 1986 | lld:pubmed |
| pubmed-article:3004227 | pubmed:articleTitle | Coxsackievirus B-3 myocarditis. Identification of different pathogenic mechanisms in DBA/2 and Balb/c mice. | lld:pubmed |
| pubmed-article:3004227 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:3004227 | pubmed:publicationType | Comparative Study | lld:pubmed |
| pubmed-article:3004227 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:3004227 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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