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T lymphocyte regulation by the adapt...

Donlin, Laura Theresa.

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T lymphocyte regulation by the adaptor molecule Sin.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	T lymphocyte regulation by the adaptor molecule Sin./
作者:	Donlin, Laura Theresa.
面頁冊數:	114 p.
附註:	Source: Dissertation Abstracts International, Volume: 65-04, Section: B, page: 1762.
Contained By:	Dissertation Abstracts International65-04B.
標題:	Health Sciences, Immunology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3128943
ISBN:	0496762036

T lymphocyte regulation by the adaptor molecule Sin.
Donlin, Laura Theresa.

T lymphocyte regulation by the adaptor molecule Sin. - 114 p.

Source: Dissertation Abstracts International, Volume: 65-04, Section: B, page: 1762.

Thesis (Ph.D.)--Columbia University, 2004.

T lymphocytes are a subclass of white blood cells that participate in adaptive immune responses. These cells develop in the thymus where they undergo a complex selection process. The T lymphocyte population that matures and migrates to the periphery is capable of identifying and attacking millions of potential foreign pathogens, while not reacting to the body's own tissue. This study investigates the manner in which one gene product, the adaptor protein Sin, regulates T lymphocyte physiology. We have demonstrated that overexpression of Sin in T lymphocytes negatively regulates T lymphocyte development, resulting in increased apoptosis. Overexpressed Sin also inhibits T lymphocyte activation by downregulating T cell receptor (TCR)-induced IL-2 production and proliferation. We have established a molecular mechanism by which this can occur---Sin inhibits the activity of PLC-gamma in the TCR signaling cascade. This inhibition occurs when Sin is phosphorylated by the Src kinase Fyn. Inhibition of PLC-gamma activity downregulates IL-2 production and subsequent T cell proliferation. Generation and initial analysis of Sin-deficient mice, however, demonstrate that endogenous Sin is not essential to the development and activation of T lymphocytes. Further studies may reveal a specific role for endogenous Sin in T lymphocyte physiology. Additionally, we have demonstrated high Sin expression levels in thymic stroma. This is consistent with recently published data demonstrating high levels of Sin expression in medullary thymic epithelial cells, which are responsible for deleting T lymphocytes that can induce autoimmune reactions. Thus, we conclude that Sin may regulate T lymphocytes on two distinct levels: first, through regulation of T lymphocyte signal transduction and second, through expression in epithelial cells that coordinate T lymphocyte development.

ISBN: 0496762036Subjects--Topical Terms:

1017716
Health Sciences, Immunology.

T lymphocyte regulation by the adaptor molecule Sin.
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520 $a T lymphocytes are a subclass of white blood cells that participate in adaptive immune responses. These cells develop in the thymus where they undergo a complex selection process. The T lymphocyte population that matures and migrates to the periphery is capable of identifying and attacking millions of potential foreign pathogens, while not reacting to the body's own tissue. This study investigates the manner in which one gene product, the adaptor protein Sin, regulates T lymphocyte physiology. We have demonstrated that overexpression of Sin in T lymphocytes negatively regulates T lymphocyte development, resulting in increased apoptosis. Overexpressed Sin also inhibits T lymphocyte activation by downregulating T cell receptor (TCR)-induced IL-2 production and proliferation. We have established a molecular mechanism by which this can occur---Sin inhibits the activity of PLC-gamma in the TCR signaling cascade. This inhibition occurs when Sin is phosphorylated by the Src kinase Fyn. Inhibition of PLC-gamma activity downregulates IL-2 production and subsequent T cell proliferation. Generation and initial analysis of Sin-deficient mice, however, demonstrate that endogenous Sin is not essential to the development and activation of T lymphocytes. Further studies may reveal a specific role for endogenous Sin in T lymphocyte physiology. Additionally, we have demonstrated high Sin expression levels in thymic stroma. This is consistent with recently published data demonstrating high levels of Sin expression in medullary thymic epithelial cells, which are responsible for deleting T lymphocytes that can induce autoimmune reactions. Thus, we conclude that Sin may regulate T lymphocytes on two distinct levels: first, through regulation of T lymphocyte signal transduction and second, through expression in epithelial cells that coordinate T lymphocyte development.
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