NDLI: TRAIL-expressing T cells induce apoptosis of vascular smooth muscle cells in the atherosclerotic plaque

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TRAIL-expressing T cells induce apoptosis of vascular smooth muscle cells in the atherosclerotic plaque

Content Provider	Semantic Scholar
Author	Sato, Kayoko Niessner, Alexander Kopecky, Stephen Louis Goronzy, Jörg J. Weyand, Cornelia M.
Copyright Year	2006
Abstract	Acute coronary syndromes (ACS) are precipitated by a rupture of the atherosclerotic plaque, often at the site of T cell and macrophage infiltration. Here, we show that plaque-infiltrating CD4 T cells effectively kill vascular smooth muscle cells (VSMC). VSMCs sensitive to T cell-mediated killing express the death receptor DR5 (TNF-related apoptosis-inducing ligand [TRAIL] receptor 2), and anti-TRAIL and anti-DR5 antibodies block T cell-mediated apoptosis. CD4 T cells that express TRAIL upon stimulation are expanded in patients with ACS and more effectively induce VSMC apoptosis. Adoptive transfer of plaque-derived CD4 T cells into immunodeficient mice that are engrafted with human atherosclerotic plaque results in apoptosis of VSMCs, which was prevented by coadministration of anti-TRAIL antibody. These data identify that the death pathway is triggered by TRAIL-producing CD4 T cells as a direct mechanism of VSMC apoptosis, a process which may lead to plaque destabilization.
Starting Page	239
Ending Page	250
Page Count	12
File Format	PDF HTM / HTML
PubMed reference number	16418392
Volume Number	203
Journal	The Journal of experimental medicine
Alternate Webpage(s)	https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/05/bf/jem2030239.PMC2118078.pdf
Alternate Webpage(s)	http://ftp.ncbi.nlm.nih.gov/pub/pmc/05/bf/jem2030239.PMC2118078.pdf
Language	English
Access Restriction	Open
Subject Keyword	Acute Coronary Syndrome Apoptosis Atherosclerosis Dental Plaque Immunologic Deficiency Syndromes Infiltration Ligands Muscle, Smooth, Vascular Patients Plaque, Atherosclerotic Rupture Senile Plaques Smooth muscle (tissue) T-Lymphocyte
Content Type	Text
Resource Type	Article

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