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Mechanisms and manipulations of auto...

Urbanek, Irene Louise.

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Mechanisms and manipulations of autoimmune disease in the NOD mouse.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	Mechanisms and manipulations of autoimmune disease in the NOD mouse./
作者:	Urbanek, Irene Louise.
面頁冊數:	144 p.
附註:	Adviser: C. Garrison Fathman.
Contained By:	Dissertation Abstracts International63-01B.
標題:	Health Sciences, Immunology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3040076
ISBN:	0493534016

Mechanisms and manipulations of autoimmune disease in the NOD mouse.
Urbanek, Irene Louise.

Mechanisms and manipulations of autoimmune disease in the NOD mouse. - 144 p.

Adviser: C. Garrison Fathman.

Thesis (Ph.D.)--Stanford University, 2002.

Human insulin-dependent diabetes mellitus (IDDM) is an autoimmune disease characterized by immune-mediated destruction of the pancreatic islets of Langerhans. The non-obese diabetic (NOD) mouse demonstrates many of the pathological features of human IDDM, and thus serves as an excellent animal model of the disease. In this work we have examined the early infiltration of the islets in order to better understand how the cascade of events which lead to autoimmunity is initiated. Our experiments provide evidence that initiation of insulitis is mediated by a single T cell clone, whose selection is likely driven by developmental conditions as well as by antigen specificity. Since it is clear that T cell trafficking is mediated by a complex network of adhesion molecules, chemokines, and chemokine receptors which coordinately direct the movement of lymphocytes, we undertook an examination of these interactions in the NOD mouse. Our data provide evidence for a central role for chemokines and their receptors in autoimmune IDDM in the NOD mouse.

ISBN: 0493534016Subjects--Topical Terms:

1017716
Health Sciences, Immunology.

Mechanisms and manipulations of autoimmune disease in the NOD mouse.
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245 1 0 $a Mechanisms and manipulations of autoimmune disease in the NOD mouse.
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500 $a Adviser: C. Garrison Fathman.
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502 $a Thesis (Ph.D.)--Stanford University, 2002.
520 $a Human insulin-dependent diabetes mellitus (IDDM) is an autoimmune disease characterized by immune-mediated destruction of the pancreatic islets of Langerhans. The non-obese diabetic (NOD) mouse demonstrates many of the pathological features of human IDDM, and thus serves as an excellent animal model of the disease. In this work we have examined the early infiltration of the islets in order to better understand how the cascade of events which lead to autoimmunity is initiated. Our experiments provide evidence that initiation of insulitis is mediated by a single T cell clone, whose selection is likely driven by developmental conditions as well as by antigen specificity. Since it is clear that T cell trafficking is mediated by a complex network of adhesion molecules, chemokines, and chemokine receptors which coordinately direct the movement of lymphocytes, we undertook an examination of these interactions in the NOD mouse. Our data provide evidence for a central role for chemokines and their receptors in autoimmune IDDM in the NOD mouse.
520 $a Current treatment of IDDM is limited to insulin therapy, which does not effectively prevent long-term complications and disability. Therefore new avenues are being explored for therapy of IDDM. Manipulation of the cytokine milieu can dramatically alter the course of an ongoing immune response, and retroviral-mediated gene therapy may be the means to such an end. Our work demonstrates that islet-specific T cells transduced with regulatory cytokines can prevent diabetes, and even ameliorate existing disease, in the NOD mouse. A second type of gene therapy is provided by immunization with plasmid DNA. We showed that plasmid DNA encoding the immunodominant peptide of insulin—amino acids 9–23 of the B chain—can prevent diabetes in NOD mice. Furthermore, administration of the vaccine to older mice at a stage when insulitis is rampant was still effective. Thus retroviral transduction with regulatory cytokine genes and/or DNA vaccination may provide viable therapies for IDDM.
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