| pubmed-article:16344296 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16344296 | lifeskim:mentions | umls-concept:C0018894 | lld:lifeskim |
| pubmed-article:16344296 | lifeskim:mentions | umls-concept:C0004153 | lld:lifeskim |
| pubmed-article:16344296 | lifeskim:mentions | umls-concept:C0079189 | lld:lifeskim |
| pubmed-article:16344296 | lifeskim:mentions | umls-concept:C0332875 | lld:lifeskim |
| pubmed-article:16344296 | pubmed:issue | 962 | lld:pubmed |
| pubmed-article:16344296 | pubmed:dateCreated | 2005-12-13 | lld:pubmed |
| pubmed-article:16344296 | pubmed:abstractText | There is growing evidence regarding the importance of inflammation in the pathogenesis of atherosclerosis and its ultimate progression to the clinical syndromes. Recently there has been an increasing interest in the role of helper T (Th) cells in atherosclerosis. The Th cells act with the macrophages and the dendritic cells via the various cytokines in bringing about a variety of changes thus leading to the progression of atherosclerosis. Atherosclerotic lesions have been seen to have increased expression of type 1 helper T (TH1) cells together with increased levels of the Th1 related cytokines. It is mainly the cytokines involved with Th1 functioning that seem to show a prominent effect, with the whole process centred around interferon gamma, making it seem like every pathway and the cytokines involved lead to a final common pathway of interferon gamma secretion; the increase or decrease of which dictates the progression of atherosclerosis and its final manifestation as the clinical syndromes. | lld:pubmed |
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