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Immune mechanisms of protection in t...

Perdow Hickman, Somia.

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Immune mechanisms of protection in tuberculosis.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	Immune mechanisms of protection in tuberculosis./
作者:	Perdow Hickman, Somia.
面頁冊數:	140 p.
附註:	Adviser: Padmini Salgame.
Contained By:	Dissertation Abstracts International63-01B.
標題:	Biology, Microbiology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3040354
ISBN:	0493536965

Immune mechanisms of protection in tuberculosis.
Perdow Hickman, Somia.

Immune mechanisms of protection in tuberculosis. - 140 p.

Adviser: Padmini Salgame.

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

With one-third of the world's population infected with <italic>Mycobacterium tuberculosis</italic>, tuberculosis remains a major threat to public health. <italic> M. tuberculosis</italic> has developed numerous mechanism for invading, surviving, and growing within the macrophage. Th1 cellular responses are important for protection against tuberculosis. However, the mechanism and antigen-presenting cell types responsible for initiation of Th1 responses are not well understood. In this study therefore, we used the murine system to examine: (1) the mechanisms that initiate Th1-mediated cellular responses, and (2) the mechanism that mediate protection.

ISBN: 0493536965Subjects--Topical Terms:

1017734
Biology, Microbiology.

Immune mechanisms of protection in tuberculosis.
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500 $a Source: Dissertation Abstracts International, Volume: 63-01, Section: B, page: 0167.
502 $a Thesis (Ph.D.)--Temple University, 2002.
520 $a With one-third of the world's population infected with <italic>Mycobacterium tuberculosis</italic>, tuberculosis remains a major threat to public health. <italic> M. tuberculosis</italic> has developed numerous mechanism for invading, surviving, and growing within the macrophage. Th1 cellular responses are important for protection against tuberculosis. However, the mechanism and antigen-presenting cell types responsible for initiation of Th1 responses are not well understood. In this study therefore, we used the murine system to examine: (1) the mechanisms that initiate Th1-mediated cellular responses, and (2) the mechanism that mediate protection.
520 $a In addition to macrophages, dendritic cells can phagocytose <italic> M. tuberculosis</italic>. Furthermore, recent studies have shown that both antigen presenting cell (APC) types are present in the lung, are found to be activated following <italic>M. tuberculosis</italic> infection, and can potentially regulate the polarization of naïve T cells. Our studies show that macrophages and dendritic cells, albeit both being antigen presenting cells, respond differently following <italic>M. tuberculosis</italic> infection and thereby have different consequences on the development of naïve T cells. We report that <italic>M. tuberculosis</italic> infected dendritic cells bias the polarization of Ova peptide-specific naïve transgenic T cells to the Th1 phenotype. In the presence of infected macrophages however, naïve T cells do not develop a Th1 phenotype. Comparison of the cytokine profile expressed by the infected dendritic cells and macrophages revealed several differences, with the most striking being that infected macrophages did not express the Th1-promoting cytokine IL-12. These studies also show that IL-10 is responsible for the failure of IL-12 production by <italic> M. tuberculosis</italic>-infected macrophages, and that the effects of IL-10 can be overcome by IFN-γ priming.
520 $a The ability of <italic>M. tuberculosis</italic> to persist in their host is thought to be a reflection of two mutually supportive strategies: (1) the avoidance or minimizing of a productive immune response, and (2) the suppression of the effector cells or cytokines that are mobilized once the response has developed. Therefore, in the present study we wanted to characterize observable differences present in the relatively susceptible BALB/C mouse strain and relatively resistant C57BL/6 strain in response to <italic>M. tuberculosis </italic> infection. We report that the BALB/C and C57BL/6 strains displayed similar kinetics of induction for NOS2, the macrophage and T cell recruitment-specific chemokines, as well as the Th1 promoting cytokines IL-12 and IFN-γ. Despite these similarities, examination of the lungs of 13-week infected mice, revealed the inability of the BALB/C mice to maintain protective granuloma architecture. This phenotype appears to correlate with enhanced apoptosis.
520 $a The goal of this thesis was to characterize the antigen presenting cell most likely responsible for initiating Th1 cell polarization, and to characterize the immunological elements that may be involved in protective immune responses. From this study, we identified the dendritic cell as the most likely candidate for initializing Th1 cellular responses in tuberculosis. From the <italic> in vivo</italic> studies, we postulate that the selective apoptosis of Th1 cells may be one mechanism of susceptibility in BALB/C mice.
590 $a School code: 0225.
650 4 $a Biology, Microbiology. $3 1017734
650 4 $a Health Sciences, Immunology. $3 1017716
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