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The role of CD4+ T cells in preventi...

Nikiforow, Sarah.

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The role of CD4+ T cells in preventing Epstein-Barr virus-induced B cell proliferation.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	The role of CD4+ T cells in preventing Epstein-Barr virus-induced B cell proliferation./
作者:	Nikiforow, Sarah.
面頁冊數:	268 p.
附註:	Source: Dissertation Abstracts International, Volume: 65-03, Section: B, page: 1235.
Contained By:	Dissertation Abstracts International65-03B.
標題:	Health Sciences, Immunology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3125272
ISBN:	0496725629

The role of CD4+ T cells in preventing Epstein-Barr virus-induced B cell proliferation.
Nikiforow, Sarah.

The role of CD4+ T cells in preventing Epstein-Barr virus-induced B cell proliferation. - 268 p.

Source: Dissertation Abstracts International, Volume: 65-03, Section: B, page: 1235.

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

Epstein-Barr virus (EBV) causes lymphoproliferative diseases and malignancies in humans because of its ability to infect and transform B cells. In healthy individuals, the immune system controls this infection and prevents outgrowth of EBV-infected B cells. In immunocompromised individuals, who lack functional T cells needed to prevent viral reactivation and outgrowth of infected B cells, EBV frequently causes B cell lymphomas. Previous studies of the immune response to EBV have focused on the activity of CD8+ T cells. While CD4+ T cells have a well-known role as helper cells, their role as cytotoxic effectors is less established. In experiments described in this dissertation, I investigated the role that effector CD4+ T cells play in preventing the early proliferation of B cells infected by EBV.

ISBN: 0496725629Subjects--Topical Terms:

1017716
Health Sciences, Immunology.

The role of CD4+ T cells in preventing Epstein-Barr virus-induced B cell proliferation.
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245 1 4 $a The role of CD4+ T cells in preventing Epstein-Barr virus-induced B cell proliferation.
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520 $a Epstein-Barr virus (EBV) causes lymphoproliferative diseases and malignancies in humans because of its ability to infect and transform B cells. In healthy individuals, the immune system controls this infection and prevents outgrowth of EBV-infected B cells. In immunocompromised individuals, who lack functional T cells needed to prevent viral reactivation and outgrowth of infected B cells, EBV frequently causes B cell lymphomas. Previous studies of the immune response to EBV have focused on the activity of CD8+ T cells. While CD4+ T cells have a well-known role as helper cells, their role as cytotoxic effectors is less established. In experiments described in this dissertation, I investigated the role that effector CD4+ T cells play in preventing the early proliferation of B cells infected by EBV.
520 $a Polyclonal memory CD4+ T cells from EBV-seropositive donors were capable of preventing early outgrowth of EBV-infected B cells in vitro in the absence of CD8+ T cells. This was demonstrated using a functional, quantitative, and reproducible assay based on the expression of CD23 by B cells undergoing latent EBV infection. Polyclonal CD4+ T cells with this activity developed in two donors within one month of their manifesting symptoms of infectious mononucleosis. Cloned CD4+ T cells reactive to the latent EBV nuclear antigen EBNA1 could prevent early outgrowth of EBV-infected CD23+ B cells from MHC class II-matched individuals and lyse fully transformed, MHC class II-matched LCLs via a Fas/Fas ligand-dependent mechanism. The ability of individual EBNA1-specific CD4+ T cell clones to recognize EBV-transformed B lymphoblastoid lines correlated with control over newly EBV-infected B cells and appeared to be influenced by the nature of the antigen-presenting cell and EBNA1 antigen used to initially expand the clones.
520 $a These results reveal that EBV-specific effector CD4+ T cells can prevent in vitro proliferation of B cells newly infected by EBV. I hypothesize that, in vitro, CD4 + T cells prevent early outgrowth of CD23+ B cells, while CD8+ T cells act later in the course of infection. The role of effector CD4+ T cells specific for EBV-infected B cells in vivo remains unknown. However, if the in vitro events mirror those which occur in vivo, polyclonal CD4 + T cells and EBNA1-specific CD4+ T cell clones may be of use as clinical adoptive immunotherapy against EBV-induced lymphomas.
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