The Role of TLR2 in the Pathogenesis of Kawasaki Disease
Kawasaki disease (KD) is a childhood vasculitis with a predilection for the coronary arteries (CA). The etiology of KD is unknown; however, superantigens (SAg) have been implicated. SAg-activated T cells undergo massive proliferation followed by apoptosis; conversely, in KD these T cells may persist...
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ndltd-TORONTO-oai-tspace.library.utoronto.ca-1807-324992013-11-15T04:04:01ZThe Role of TLR2 in the Pathogenesis of Kawasaki DiseaseWardinger, JaimieTLR2Kawasaki DiseaseEndothelial cells0982Kawasaki disease (KD) is a childhood vasculitis with a predilection for the coronary arteries (CA). The etiology of KD is unknown; however, superantigens (SAg) have been implicated. SAg-activated T cells undergo massive proliferation followed by apoptosis; conversely, in KD these T cells may persist and target the CAs. Enhanced costimulation can rescue SAg-activated T cells from apoptosis, and Toll-like receptor 2 (TLR2) enhances costimulation. In a murine model of KD, TLR2-deficient mice are disease resistant, and evidence suggests preferential expression of TLR2 at the CA. Results from this study demonstrate that TLR2 is rapidly expressed in the heart following disease induction, and that TLR2 is expressed differentially in various arteries. The aorta, from which the CAs branch off, expressed the highest TLR2 levels. A microvascular endothelial cell line was shown to function as an APC following TLR2 stimulation, supporting the proliferation of SAg-activated T cells and their rescue from apoptosis.Yeung, Rae S. M.2012-062012-07-23T19:12:03ZNO_RESTRICTION2012-07-23T19:12:03Z2012-07-23Thesishttp://hdl.handle.net/1807/32499en_ca |
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TLR2 Kawasaki Disease Endothelial cells 0982 |
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TLR2 Kawasaki Disease Endothelial cells 0982 Wardinger, Jaimie The Role of TLR2 in the Pathogenesis of Kawasaki Disease |
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Kawasaki disease (KD) is a childhood vasculitis with a predilection for the coronary arteries (CA). The etiology of KD is unknown; however, superantigens (SAg) have been implicated. SAg-activated T cells undergo massive proliferation followed by apoptosis; conversely, in KD these T cells may persist and target the CAs. Enhanced costimulation can rescue SAg-activated T cells from apoptosis, and Toll-like receptor 2 (TLR2) enhances costimulation. In a murine model of KD, TLR2-deficient mice are disease resistant, and evidence suggests preferential expression of TLR2 at the CA. Results from this study demonstrate that TLR2 is rapidly expressed in the heart following disease induction, and that TLR2 is expressed differentially in various arteries. The aorta, from which the CAs branch off, expressed the highest TLR2 levels. A microvascular endothelial cell line was shown to function as an APC following TLR2 stimulation, supporting the proliferation of SAg-activated T cells and their rescue from apoptosis. |
author2 |
Yeung, Rae S. M. |
author_facet |
Yeung, Rae S. M. Wardinger, Jaimie |
author |
Wardinger, Jaimie |
author_sort |
Wardinger, Jaimie |
title |
The Role of TLR2 in the Pathogenesis of Kawasaki Disease |
title_short |
The Role of TLR2 in the Pathogenesis of Kawasaki Disease |
title_full |
The Role of TLR2 in the Pathogenesis of Kawasaki Disease |
title_fullStr |
The Role of TLR2 in the Pathogenesis of Kawasaki Disease |
title_full_unstemmed |
The Role of TLR2 in the Pathogenesis of Kawasaki Disease |
title_sort |
role of tlr2 in the pathogenesis of kawasaki disease |
publishDate |
2012 |
url |
http://hdl.handle.net/1807/32499 |
work_keys_str_mv |
AT wardingerjaimie theroleoftlr2inthepathogenesisofkawasakidisease AT wardingerjaimie roleoftlr2inthepathogenesisofkawasakidisease |
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1716614129600430080 |