Linked Life Data

10851260

Source:http://linkedlifedata.com/resource/pubmed/id/10851260

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2000-8-21
pubmed:abstractText
It is now well established that immune effector mechanisms contribute to cardiac dysfunction in several heart diseases, including myocarditis and the associated dilated cardiomyopathy, heart transplant rejection and Chagas' disease. These and other pathologies, in which cellular immunity plays an important role, contribute to morbidity and mortality world-wide. As a result of numerous studies performed in this exciting field, two major mechanisms of lymphocytotoxicity have been proposed: a secretory mechanism in which perforin and granzymes are key players, and a non-secretory mechanism involving Fas/FasL activation. While the common notion is that CTL-myocyte interaction, perforin- or Fas-based, inevitably results in target cell apoptotic death, the objective of this review is to consider the concept of non-apoptotic consequences of CTL-target cell interaction. It is proposed that depending on the myocyte status as well as on the fine balance between pro- and anti-apoptotic factors, CTL-myocyte interaction may result in a non-apoptotic, potentially reversible sustained damage to the myocytes, thus contributing to immune-mediated cardiac dysfunction.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
1107-3756
pubmed:author
pubmed:issnType
Print
pubmed:volume
6
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3-16
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
2000
pubmed:articleTitle
Immune effector mechanisms in myocardial pathologies.
pubmed:affiliation
Rappaport Institute, P.O. Box 9697, Haifa 31096, Israel.
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't