Linked Life Data

12086261

Source:http://linkedlifedata.com/resource/pubmed/id/12086261

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2002-6-27
pubmed:abstractText
T lymphocytes, encountering stimulatory signals in the adventitia of medium-size arteries, emerge as the key players in inflammation-associated injury pathways. In GCA, all injury mechanisms have been related to effector macrophages. Regulated by IFN-gamma-producing T cells, macrophages commit to distinct avenues of differentiation and acquire a spectrum of potentially harmful capabilities (Figure 1). Macrophages in the adventitia focus on production of pro-inflammatory cytokines. Macrophages in the media specialize in oxidative damage with lipid peroxidation attacking smooth muscle cells and matrix components. These macrophages also supply reactive oxygen intermediates that, in combination with nitrogen intermediates, cause protein nitration of endothelial cells. Production of oxygen radicals is complemented by the production of metalloproteinases, likely essential in the breakdown of elastic membranes. With the fragmentation of the internal elastic lamina, the intimal layer becomes accessible to migratory myofibroblasts that, driven by PDGF, form a hyperplastic intimal layer and cause occlusion of the vessel lumen. Expansion of the hyperplastic intima is accompanied by intense neoangiogenesis, supported by angiogenesis factors that again derive from specialized macrophages. Similarities in injury pathways between GCA and another arterial disease, atherosclerosis, are beginning to be recognized. Specifically, activated T cells and macrophages are increasingly appreciated as key players in the process of instability and rupture of atherosclerotic plaque. A specialized subset of CD4 T cells, CD4+ CD28- T cells, are suspected to participate in tissue injury in the plaque. These T cells are equipped with cytolytic capabilities and release large amounts of IFN-gamma. Comparative studies between patients with GCA and those with acute coronary syndromes should enhance our ability to define the principles of arterial wall inflammation, the specifics of injury in that microenvironment, and help in the identification of the eliciting signals.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0891-1150
pubmed:author
pubmed:issnType
Print
pubmed:volume
69 Suppl 2
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
SII28-32
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
2002
pubmed:articleTitle
Pathogenic mechanisms in giant cell arteritis.
pubmed:affiliation
Department of Medicine, Mayo Medical and Graduate Schools, Rochester, MN, USA. weyand.cornelia@mayo.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Review, Research Support, Non-U.S. Gov't