Recent evidence suggests that an inflammatory process has a significant role in the evolution of atherosclerosis. A chronic inflammatory response in the blood vessel's wall causes the formation of a lesion that narrows the artery's lumen and may cause such conditions as stable angina (SA). Destabilization of the atheromatous lesion, blood clot formation and rapid narrowing of the artery lumen may appear as part of an acute process, superimposed on the chronic inflammation, Such an acute process may be the mechanism underlying acute conditions such as unstable angina (UA) or myocardial infarction. Recent studies are trying to shed light on the process which causes destabilization of the atheromatous lesion. These studies implicate T lymphocytes and, especially, T helper 1 (Th1) cells (a sub-population of T lymphocytes) as having an important role in the destabilization of the lesion. Interferon γ, an important cytokine secreted by Th1 cells, diminishes the production of collagen by smooth muscle cells and activates macrophages which destroy collagen and elastin. Furthermore, interferon γ encourages clot formation and disrupts production of nitric oxide by endothelial cells. These qualities of interferon γ support the hypothesis by which Th1 cells play a significant role in the evolution of UA. Unlike Th1 cells, Th2 cells, another sub-population of T lymphocytes, may help protect the atheromatous lesion from destabilization. This hypothesis is supported by the qualities of interleukin 10, one of the important cytokine secreted by Th2 cells. Interleukin 10 diminishes the secretion of interferon-γ, inhibits the secretion of enzymes which destroy connective tissue in the atheromatous lesion and interferes with clot formation on the unstable lesion.
|State||Published - 1 Sep 2003|
- Interferon γ
- Interleukin 10
- Unstable angina