doi: 10.1161/01.ATV.0000154921.49792.ef
© 2005 American Heart Association, Inc.
Editorials |
When Interleukin-18 Conducts, the Preludio Sounds the Same no Matter Who Plays
From INSERM EMI 0016, Medicine Faculty (G.C.), Paris V University, and UPMC and INSERM U681 (S.K., A.N.), Cordeliers Institute, Paris, France
Correspondence to Giuseppina Caligiuri, INSERM EMI 00-16, Sixth Floor porte 2, Faculté de Médecine Necker-Enfants Malades, Paris, Cedex 15, France. E-mail caligiuri@necker.fr
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
The first event in atherogenesis is the extravasation of lipoproteins into the subintimal layers of arteries, where they are trapped by extracellular matrix molecules such as proteoglycans and undergo oxidative modifications that in turn lead to endothelial cell activation and local recruitment of inflammatory cells. The monocyte-derived macrophages transform into foam cells by an unlimited upload of oxidized lipoproteins. Foam cells accumulated in the subintimal space constitute the fatty streaks. During this process, macrophages become activated and release a number of cytokines and proteases, which perpetuate the local inflammatory environment. It is now recognized that such a chronic inflammatory process is the fundamental pathogenic mechanism of atherogenesis. In this issue of Arteriosclerosis, Thrombosis, and Vascular Biology, Tenger et al address the role of a key molecule, interleukin (IL)-18, in the regulation of this inflammatory condition.1
See page 791
In recent years, the role of the adaptive immune response, evoked by activated T cells present within the plaque, has attracted growing attention. Experimental studies have confirmed that B and T cells play a modulatory role in atherogenesis. On one hand, B cell response is atheroprotective.2 On the other, fully immunodeficient proatherosclerotic mice develop substantially smaller lesions than do immunocompetent siblings.3,4 Reconstitution with CD4+ T cells alone reestablishes full-blown atherosclerotic plaques in immunodeficient mice.4 As a consequence, a number of studies have focused on the mechanisms by which T cells are activated and become pathogenic in atherosclerosis. It has been proposed that pathogenicity of T cells is conferred by a proinflammatory
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and CXCL16 Expression Independently of T Cells
Arterioscler Thromb Vasc Biol 2005 25: 791-796.
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