doi: 10.1161/01.ATV.0000237564.81178.bb
© 2006 American Heart Association, Inc.
Editorials |
IL-20 and Atherosclerosis
Another Brick In the Wall
From INSERM UMRS 681, Université Pierre et Marie Curie Paris 6, Institut de Recherches Biomédicales des Cordeliers, France.
Correspondence to Giuseppina Caligiuri, INSERM UMRS 681, Université Pierre et Marie Curie Paris 6, Institut de Recherches Biomédicales des Cordeliers, 15, rue de l’Ecole de Médecine, 75006 Paris, France. E-mail giuseppina.caligiuri@umrs681.jussieu.fr
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Achronic inflammatory process, initiated by lipoprotein extravasation and oxidation in the intimal space, builds up atherosclerotic plaques in the arterial wall.
See page 2090
Cytokines are fundamental actors of inflammation as they exert autocrine and paracrine effects and allow intercellular communication between effector and target cells. More than fifty cytokines have been identified by now. Shortly after their discovery, novel and unexpected biological actions of cytokines are brought to light by cross-disciplinary studies.
Thus, the intersection between the cardiovascular and the immunology research fields has prompted an increasing number of studies focusing on the identification of either proatherogenic or antiatherogenic effects of cytokines (please see Tedgui and Mallat 1 for extensive review).
Blumberg et al2 have used a bioinformatics algorithm designed to identify helical cytokines, which has allowed them to discover a novel cytokine, interleukin (IL)-20. The authors determined that its heterodimeric receptor is structurally related to the IL-10 receptor and therefore assigned IL-20 to the IL-10 subfamily within class II cytokines.1 Nevertheless, concurrently with its discovery, Blumberg et al have demonstrated that the biological activity of IL-20 in skin and its role in psoriasis is opposite to that of IL-10.2
In this issue of Arteriosclerosis, Thrombosis, and Vascular Biology, Chen et al show that IL-20 and its receptors are expressed in human and experimental atherosclerotic plaques. More importantly, the authors demonstrate that systemic delivery of IL-20 accelerates atherogenesis in the apolipoprotein E–knockout mouse model.3
Thus, as in the case of psoriasis, the role of IL-20 appears to be opposite
Related Article:
Arterioscler Thromb Vasc Biol 2006 26: 2090-2095.
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