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Wrong Harley Tse?

Harley Y. Tse

Professor and Deputy Chair, Department of Immunology and Microbiology

Wayne State University

HQ Phone:  (313) 577-4449

Direct Phone: (313) ***-****direct phone

Email: h***@***.edu

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I agree to the Terms of Service and Privacy Policy. I understand that I will receive a subscription to ZoomInfo Community Edition at no charge in exchange for downloading and installing the ZoomInfo Contact Contributor utility which, among other features, involves sharing my business contacts as well as headers and signature blocks from emails that I receive.

Wayne State University

5057 Woodward Avenue Suite 3101

Detroit, Michigan,48202

United States

Company Description

Wayne State University is one of the nation's pre-eminent public research universities in an urban setting. Through its multidisciplinary approach to research and education, and its ongoing collaboration with government, industry and other institutions, the un...more

Background Information

Employment History

Editor

iMed Pub LLC


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Associate Professor of Immunology and Microbiology

WSU's School of Medicine


Affiliations

Merck Sharp and Dohme Research Laboratories

Research Fellow


Education

Ph.D.


Web References(13 Total References)


www.imedpub.com

Harley Y. Tse, Professor and Deputy Chair, Department of Immunology and Microbiology, Wayne State University School of Medicine, USA


ohcampus.com

The vaccine could also target strokes which are a product of plaque buildup in arteries," said Harley Tse, a professor of immunology and microbiology in Wayne State University's school of medicine.
Shaw and Tse demonstrated that two T cell epitopes of the autoantigen "apoB100 are deeply involved in the development of the disease. Although T-cells of the immune system are known to participate in the development of heart disease, by what and how these T-cells are directed to act has not been elucidated. "With the discovery of the disease-causing T-cell epitopes, we can now manipulate the activities of the T-cells responding to these epitopes to control the disease," Shaw said. Shaw and Tse conceptualised that finding the "apoB100 epitopes capable of stimulating the disease causing (atherogenic) T-cells is a prerequisite to understand how these T-cells are involved in heart disease development and how to control their adverse effects. They identified two short sequences of "apoB100 that were able to direct specific T-cells to proliferate as well as to cause worsening atherosclerosis. "This discovery is significant because it identifies the target T-cells and makes it possible to manipulate this population of pathologic T-cells away from their harmful activities," Shaw and Tse said.


www.dailypioneer.com

The vaccine could also target strokes which are a product of plaque buildup in arteries," said Harley Tse, a professor of immunology and microbiology in Wayne State University's school of medicine.
Shaw and Tse demonstrated that two T cell epitopes of the autoantigen "apoB100" are deeply involved in the development of the disease. Although T-cells of the immune system are known to participate in the development of heart disease, by what and how these T-cells are directed to act has not been elucidated. "With the discovery of the disease-causing T-cell epitopes, we can now manipulate the activities of the T-cells responding to these epitopes to control the disease," Shaw said. Shaw and Tse conceptualised that finding the "apoB100" epitopes capable of stimulating the disease causing (atherogenic) T-cells is a prerequisite to understand how these T-cells are involved in heart disease development and how to control their adverse effects. They identified two short sequences of "apoB100" that were able to direct specific T-cells to proliferate as well as to cause worsening atherosclerosis. "This discovery is significant because it identifies the target T-cells and makes it possible to manipulate this population of pathologic T-cells away from their harmful activities," Shaw and Tse said. The novel discovery is reported in the Journal of Immunology and Clinical Research.


www.deccanherald.com

The vaccine could also target strokes which are a product of plaque buildup in arteries," said Harley Tse, a professor of immunology and microbiology in Wayne State University's school of medicine.
Shaw and Tse demonstrated that two T cell epitopes of the autoantigen "apoB100" are deeply involved in the development of the disease. Although T-cells of the immune system are known to participate in the development of heart disease, by what and how these T-cells are directed to act has not been elucidated. "With the discovery of the disease-causing T-cell epitopes, we can now manipulate the activities of the T-cells responding to these epitopes to control the disease," Shaw said. Shaw and Tse conceptualised that finding the "apoB100" epitopes capable of stimulating the disease causing (atherogenic) T-cells is a prerequisite to understand how these T-cells are involved in heart disease development and how to control their adverse effects. They identified two short sequences of "apoB100" that were able to direct specific T-cells to proliferate as well as to cause worsening atherosclerosis. "This discovery is significant because it identifies the target T-cells and makes it possible to manipulate this population of pathologic T-cells away from their harmful activities," Shaw and Tse said.


www.eurekalert.org

The published work, performed in the laboratory of Klaus Ley, M.D., a prominent vascular biologist of LIAI, was based on the fundamental discovery made by Harley Tse, Ph.D., professor of immunology and microbiology in Wayne State's School of Medicine, and professor in Wayne State's Cardiovascular Research Institute, and Michael Shaw, Ph.D., adjunct assistant professor of immunology and microbiology at Wayne State.
Shaw and Tse are the first to demonstrate that two T cell epitopes of the autoantigen apoB100 are deeply involved in the development of the disease. "ApoB100 is an apolipoprotein of the LDL (low-density lipoprotein) particle which is the notorious 'bad cholesterol' that contributes to the formation of plaques in the vessel wall," said Tse. "Although T cells of the immune system are known to participate in the development of heart disease, by what and how these T cells are directed to act have not been elucidated. The lack of this knowledge has greatly hampered the development of immune peptide-based therapeutics to control the disease. With the discovery of the disease-causing T cell epitopes, we can now manipulate the activities of the T cells responding to these epitopes to control the disease." Since immune T cells are normally activated by a short sequence (called an epitope), and not by the whole molecule of an antigen, Shaw and Tse conceptualized that finding the apoB100 epitopes capable of stimulating the disease causing (atherogenic) T cells is a prerequisite for understanding how these T cells are involved in heart disease development and for finding ways to control their adverse effects. Substantial funding for Dr. Tse's research was provided by the Office of the Vice President for Research at Wayne State University.


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