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Influences of B7 costimulation in in...

Thebeau, Lydia Gayle.

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Influences of B7 costimulation in induction of immune responses to HSV-2 and attenuation of pathology.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	Influences of B7 costimulation in induction of immune responses to HSV-2 and attenuation of pathology./
作者:	Thebeau, Lydia Gayle.
面頁冊數:	146 p.
附註:	Adviser: Lynda A. Morrison.
Contained By:	Dissertation Abstracts International63-05B.
標題:	Health Sciences, Immunology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3051849
ISBN:	0493668209

Influences of B7 costimulation in induction of immune responses to HSV-2 and attenuation of pathology.
Thebeau, Lydia Gayle.

Influences of B7 costimulation in induction of immune responses to HSV-2 and attenuation of pathology. - 146 p.

Adviser: Lynda A. Morrison.

Thesis (Ph.D.)--Saint Louis University, 2002.

Induction of T cell-mediated immune responses requires stimulation of the T cells by two signals: (1) engagement of the T cell receptor by antigen and MHC presented by antigen presenting cells, and (2) engagement of the T cell co-receptor CD28 with a costimulatory molecule B7-1 or B7-2. Many studies have demonstrated the importance of B7 costimulation in the generation of antigen-specific immune responses. Germline deletion of the genes encoding B7-1 and B7-2 in mice represents a genetic approach to interruption of the B7-costimulation pathway that has the advantage of completely and selectively blocking B7-1 and B7-2 interactions. Previous studies with these mice demonstrate the dependence on B7 costimulation of the antigen-specific, cytotoxic T lymphocyte and antibody responses to VSV, but due to lack of pathology in the mouse, the impact of these compromised immune responses on capacity to resist pathogen-induced disease could not be assessed.

ISBN: 0493668209Subjects--Topical Terms:

1017716
Health Sciences, Immunology.

Influences of B7 costimulation in induction of immune responses to HSV-2 and attenuation of pathology.
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520 $a Induction of T cell-mediated immune responses requires stimulation of the T cells by two signals: (1) engagement of the T cell receptor by antigen and MHC presented by antigen presenting cells, and (2) engagement of the T cell co-receptor CD28 with a costimulatory molecule B7-1 or B7-2. Many studies have demonstrated the importance of B7 costimulation in the generation of antigen-specific immune responses. Germline deletion of the genes encoding B7-1 and B7-2 in mice represents a genetic approach to interruption of the B7-costimulation pathway that has the advantage of completely and selectively blocking B7-1 and B7-2 interactions. Previous studies with these mice demonstrate the dependence on B7 costimulation of the antigen-specific, cytotoxic T lymphocyte and antibody responses to VSV, but due to lack of pathology in the mouse, the impact of these compromised immune responses on capacity to resist pathogen-induced disease could not be assessed.
520 $a We have used a highly lytic and pathogenic herpes simplex virus 2 (HSV-2) as a model system to investigate the influence of B7 costimulation on development of immune responses capable of controlling infection and disease. We have found that B7KO mice infected intravaginally with virulent HSV-2 showed more severe disease pathology and higher mortality than their wild-type counterparts. B7KO mice had significant defects in antigen-specific class-switched antibody responses in the serum. HSV specific serum IgG was significantly reduced, with 10- to 100-fold differences in IgG2a and IgG1 production, respectively. Cytokine production by T cells was impaired in B7KO mice compared to wild-type mice, and CD40L expression was depressed, suggesting a mechanism for decreased production of class-switched antibody. In the absence of B7 costimulation, naive T cells fail to undergo proper activation in response to HSV-2, which limits immune induction. This immune-compromised condition plays a role in the observed increase in susceptibility and mortality of B7KO mice to HSV-2 infection.
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