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The role of antigen compartmentaliza...

Doling, Amy Melissa.

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The role of antigen compartmentalization in the priming of CD8(+) T cells.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	The role of antigen compartmentalization in the priming of CD8(+) T cells./
作者:	Doling, Amy Melissa.
面頁冊數:	129 p.
附註:	Adviser: Michael N. Starnbach.
Contained By:	Dissertation Abstracts International63-10B.
標題:	Biology, Microbiology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3067382
ISBN:	0493867910

The role of antigen compartmentalization in the priming of CD8(+) T cells.
Doling, Amy Melissa.

The role of antigen compartmentalization in the priming of CD8(+) T cells. - 129 p.

Adviser: Michael N. Starnbach.

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

CD8<super>+</super> T cells constitute one arm of the immune system and are often required for protective immunity against intracellular pathogens. CD8<super>+</super> T cells recognize infected cells when peptide epitopes derived from these pathogens are presented by molecules encoded by the host class I major histocompatibility complex (MHC-I). CD8<super>+</super> T cells are activated through their interaction with the MHC-I:peptide complex and perform effector functions that limit the spread of the organism. In this thesis, I investigated the use of a modified non-toxic form of anthrax toxin as a delivery system designed to prime protective CD8<super>+</super> T cells. I also investigated whether CD8<super>+</super> T cells could recognize and respond to <italic>S. flexneri</italic>-infected cells.

ISBN: 0493867910Subjects--Topical Terms:

1017734
Biology, Microbiology.

The role of antigen compartmentalization in the priming of CD8(+) T cells.
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502 $a Thesis (Ph.D.)--Harvard University, 2002.
520 $a CD8<super>+</super> T cells constitute one arm of the immune system and are often required for protective immunity against intracellular pathogens. CD8<super>+</super> T cells recognize infected cells when peptide epitopes derived from these pathogens are presented by molecules encoded by the host class I major histocompatibility complex (MHC-I). CD8<super>+</super> T cells are activated through their interaction with the MHC-I:peptide complex and perform effector functions that limit the spread of the organism. In this thesis, I investigated the use of a modified non-toxic form of anthrax toxin as a delivery system designed to prime protective CD8<super>+</super> T cells. I also investigated whether CD8<super>+</super> T cells could recognize and respond to <italic>S. flexneri</italic>-infected cells.
520 $a I first investigated the use of an anthrax toxin delivery system as an immunization strategy to stimulate CD8<super>+</super> T cells. Designing CD8<super>+</super> T cell vaccines has been difficult because CD8<super> +</super> T cell antigens have to be efficiently introduced into the cytoplasm of host cells. One strategy to deliver antigens to the cytoplasm of cells is to exploit the intrinsic ability of some proteins to translocate into the cytosol. I investigated the ability of a non-toxic form of anthrax toxin to serve as a CD8<super>+</super> T cell antigen delivery vehicle. During intoxication with anthrax toxin, protective antigen (PA) directs the translocation of another protein, lethal factor (LF), into the cytoplasm of cells. As part of this thesis, I created fusion proteins between a non-toxic form of LF (LFn) and CD8<super>+</super> T cell epitopes and demonstrated that the anthrax toxin delivery system can stimulate protective CD8<super>+</super> T cells against a variety of viral and bacterial organisms.
520 $a The second aim of the work presented in this thesis was to investigate the role of CD8<super>+</super> T cells in protection against the intracellular bacterium, <italic>Shigella flexneri. S. flexneri</italic> resides within, and secretes proteins into, the cytoplasm of host cells. Therefore, it initially seemed likely that epitopes from these proteins would be presented by host MHC-I molecules and stimulate the response of CD8<super>+</super> T cells during the infection process. However, I was not able to demonstrate that CD8<super>+</super> T cells were primed against <italic>S. flexneri</italic> secreted proteins during in vivo infection of mice, nor was I able to show that cultured cells infected with <italic>S. flexneri</italic> were recognized by CD8<super>+</super> T cells <italic>in vitro</italic>. These results were surprising since <italic>S. flexneri</italic> secreted proteins should be accessible to the MHC-I processing pathway and suggested the possibility that <italic> S. flexneri</italic> was inhibiting the ability of CD8<super>+</super> T cells to recognize and/or respond to infected cells.
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