(Circulation. 1997;96:396-399.)
© 1997 American Heart Association, Inc.
Articles |
Activation of Monocyte/Macrophage Functions Related to Acute Atheroma Complication by Ligation of CD40
Induction of Collagenase, Stromelysin, and Tissue Factor
From the Vascular Medicine and Atherosclerosis Unit (F.M., U.S., P.L.), Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass; the Geneva Biomedical Research Institute (J.-Y.B.), Geneva, Switzerland; and the Molecular Cardiobiology Program, Boyer Center for Molecular Medicine (J.S.P), Yale University School of Medicine, New Haven, Conn.
Correspondence to Peter Libby, MD, Vascular Medicine and Atherosclerosis Unit, Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, 221 Longwood Ave, LMRC 307, Boston, MA 02115. E-mail plibby{at}bustoff.bwh.harvard.edu
Background Plaque disruption with thrombosis commonly causes the acute coronary syndromes. Macrophages, abundant at sites of plaque rupture, release proteinases that weaken plaques and express tissue factor (TF), which initiates thrombosis. The signals that induce expression of these macrophage functions, particularly TF, remain obscure. Recent studies have localized the receptor CD40 and its ligand in human atheroma. This study tested the hypothesis that ligation of CD40 can activate key mononuclear phagocyte functions related to clinical manifestations of atheroma.
Methods and Results Stimulation of human
monocytes/macrophages through CD40 by either membranes from
activated T cells or recombinant CD40L (rCD40L) induced
expression of interstitial collagenase,
stromelysin, and TF protein and activity. In contrast, the soluble
cytokines interleukin-1 or tumor necrosis factor-
did not
induce or weakly induced TF expression. Neutralization with anti-CD40L
antibody markedly inhibited these actions of both T-cell membranes and
rCD40L.
Conclusions By inducing the expression of matrix-degrading proteinases and of TF procoagulant, CD40 signaling may contribute to the triggering of acute coronary events.
Key Words: CD40 ligands • atheroma • thrombosis • plaque • macrophages
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R. Rabbani and E. J. Topol Strategies to achieve coronary arterial plaque stabilization Cardiovasc Res, February 1, 1999; 41(2): 402 - 417. [Abstract] [Full Text] [PDF]
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R. Ross Atherosclerosis -- An Inflammatory Disease N. Engl. J. Med., January 14, 1999; 340(2): 115 - 126. [Full Text] [PDF]
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F. Mach, U. Schonbeck, R. P. Fabunmi, C. Murphy, E. Atkinson, J.-Y. Bonnefoy, P. Graber, and P. Libby T Lymphocytes Induce Endothelial Cell Matrix Metalloproteinase Expression by a CD40L-Dependent Mechanism : Implications for Tubule Formation Am. J. Pathol., January 1, 1999; 154(1): 229 - 238. [Abstract] [Full Text] [PDF]
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 P. Libby The interface of atherosclerosis and thrombosis: basic mechanisms Vascular Medicine, August 1, 1998; 3(3): 225 - 229. [Abstract] [PDF]
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M. Aikawa, E. Rabkin, Y. Okada, S. J. Voglic, S. K. Clinton, C. E. Brinckerhoff, G. K. Sukhova, and P. Libby Lipid Lowering by Diet Reduces Matrix Metalloproteinase Activity and Increases Collagen Content of Rabbit Atheroma : A Potential Mechanism of Lesion Stabilization Circulation, June 23, 1998; 97(24): 2433 - 2444. [Abstract] [Full Text] [PDF]
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