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Blood, 1 December 2003, Vol. 102, No. 12, pp. 4052-4058. Prepublished online as a Blood First Edition Paper on August 14, 2003; DOI 10.1182/blood-2003-05-1729. This Article Full Text Full Text (PDF) All Versions of this Article: 2003-05-1729v1 102/12/4052    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Gojova, A. Articles by Groux, H. Search for Related Content PubMed PubMed Citation Articles by Gojova, A. Articles by Groux, H. Related Collections Hemostasis, Thrombosis, and Vascular Biology Immunobiology Transplantation Signal Transduction Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY Specific abrogation of transforming growth factor- signaling in T cells alters atherosclerotic lesion size and composition in mice Andrea Gojova, Valérie Brun, Bruno Esposito, Françoise Cottrez, Pierre Gourdy, Patrice Ardouin, Alain Tedgui, Ziad Mallat, and Hervé Groux From the Institut National de la Santé et de la Recherche Médicale (INSERM) U541, Institut Fédératif de Recherche "Circulation Paris VII," Hôpital Lariboisière, Paris, France; TxCell, Bâtiment. ARC and INSERM U343, Hôpital de l'Archet, Nice, France; INSERM U397, Toulouse, France; and Institut Gustave Roussy, Villejuif, France. A large body of evidence supports a role for proinflammatory mediators in atherosclerotic disease progression and instability. However, only few endogenous mechanisms have been suggested that could alter disease progression. One such mechanism is thought to be mediated by transforming growth factor (TGF-). Transgenic mice that express a dominant-negative TGF- receptor type II under a T-cell-specific promoter were generated. Bone marrow transplantation from transgenic mice into irradiated low density lipoprotein receptor knock-out (LDLr KO) mice, subsequently fed an atherogenic diet, resulted in T-cell-specific blockade of TGF- signaling in the recipient mice and increased differentiation of T cells toward both T helper 1 (Th1) and Th2 phenotypes. These mice showed a significant decrease in atherosclerotic lesion size in the aortic sinus compared with mice receiving transplants with the wild-type bone marrow. Atherosclerotic plaques of mice receiving transplants with the transgenic bone marrow showed increased T-cell infiltration and expression of major histocompatability complex (MHC) class II, along with a decrease in smooth muscle cell and collagen content, a plaque phenotype that is potentially vulnerable to rupture. These results identify for the first time an important role for specific and selective T-cell-TGF- signaling in atherosclerosis. (Blood. 2003;102:4052-4058) CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: A. D. Frutkin, G. Otsuka, A. Stempien-Otero, C. Sesti, L. Du, M. Jaffe, H. L. Dichek, C. J. Pennington, D. R. Edwards, M. Nieves-Cintron, et al. TGF-{beta}1 Limits Plaque Growth, Stabilizes Plaque Structure, and Prevents Aortic Dilation in Apolipoprotein E-Null Mice Arterioscler Thromb Vasc Biol, September 1, 2009; 29(9): 1251 - 1257. [Abstract] [Full Text] [PDF] Z. Mallat, S. Taleb, H. 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