東華大學圖書館 |

語系: 繁體中文

說明(常見問題)

回圖書館首頁

手機版館藏查詢

登入

回首頁

切換: 標籤 | MARC模式 | ISBD

Cytotoxic T lymphocyte antigen-4 reg...

Love, Victoria A.

FindBook

Google Book

Amazon

博客來

Cytotoxic T lymphocyte antigen-4 regulates cytotoxic T cells that cause myocarditis.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Cytotoxic T lymphocyte antigen-4 regulates cytotoxic T cells that cause myocarditis./
作者:	Love, Victoria A.
面頁冊數:	172 p.
附註:	Source: Dissertation Abstracts International, Volume: 67-05, Section: B, page: 2463.
Contained By:	Dissertation Abstracts International67-05B.
標題:	Biology, Cell. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3217813
ISBN:	9780542693304

Cytotoxic T lymphocyte antigen-4 regulates cytotoxic T cells that cause myocarditis.
Love, Victoria A.

Cytotoxic T lymphocyte antigen-4 regulates cytotoxic T cells that cause myocarditis. - 172 p.

Source: Dissertation Abstracts International, Volume: 67-05, Section: B, page: 2463.

Thesis (Ph.D.)--Harvard University, 2006.

Disruption of Cytotoxic T Lymphocyte antigen-4 (CTLA-4) signals either by gene ablation or reagents that prevent signaling causes a life-threatening lymphoproliferative disorder in both mice and humans. The ligands for CTLA-4 are the B7-1 (CD80) and B7-2 (CD86) co-stimulatory molecules that are upregulated on antigen-presenting cells (APC). CTLA-4 is inducible upon activation of CD4+ and CD8+ T cells. While the molecule has overlapping functions, there are non-redundant affects among these closely related, but separate T cell subsets. One obvious difference is at the level of cell cycle regulation, where CTLA-4 mediated inhibitory cues noticeably manifest during recall responses. In contrast, CTLA-4 regulates both primary and secondary activation in CD4+ cells. The mechanisms of CTLA-4 control of CD4+ cellular process are relatively well defined compared to what is known about CD8+ regulation in this context.

ISBN: 9780542693304Subjects--Topical Terms:

1017686
Biology, Cell.

Cytotoxic T lymphocyte antigen-4 regulates cytotoxic T cells that cause myocarditis.
LDR:03457nmm 2200301 4500 001 1829040
005 20071106080109.5
008 130610s2006 eng d
020 $a 9780542693304
035 $a (UMI)AAI3217813
035 $a AAI3217813
040 $a UMI $c UMI
100 1 $a Love, Victoria A. $3 1917912
245 1 0 $a Cytotoxic T lymphocyte antigen-4 regulates cytotoxic T cells that cause myocarditis.
300 $a 172 p.
500 $a Source: Dissertation Abstracts International, Volume: 67-05, Section: B, page: 2463.
500 $a Adviser: Andrew H. Lichtman.
502 $a Thesis (Ph.D.)--Harvard University, 2006.
520 $a Disruption of Cytotoxic T Lymphocyte antigen-4 (CTLA-4) signals either by gene ablation or reagents that prevent signaling causes a life-threatening lymphoproliferative disorder in both mice and humans. The ligands for CTLA-4 are the B7-1 (CD80) and B7-2 (CD86) co-stimulatory molecules that are upregulated on antigen-presenting cells (APC). CTLA-4 is inducible upon activation of CD4+ and CD8+ T cells. While the molecule has overlapping functions, there are non-redundant affects among these closely related, but separate T cell subsets. One obvious difference is at the level of cell cycle regulation, where CTLA-4 mediated inhibitory cues noticeably manifest during recall responses. In contrast, CTLA-4 regulates both primary and secondary activation in CD4+ cells. The mechanisms of CTLA-4 control of CD4+ cellular process are relatively well defined compared to what is known about CD8+ regulation in this context.
520 $a In order to assess the function of CTLA-4 in the regulation of CD8 + T cells, we generated CTLA-4-/-, Rag 2-/- , OT-1 mice whose T cells express an ovalumbin peptide-specific, class I MHC-restricted TCR. Freshly isolated CTLA-4-/- OT-I cells have a naive phenotype indistinguishable from control OT-I cells. Effector T cells were generated in vitro by stimulating CTLA-4-/- control OT-1 cells with antigen and IL-12. The CTLA-4-/- effectors proliferated significantly more than control effectors upon antigen-restimulation. Transfer of 5 x 104 CTLA-4-/- OT-I effector cells into CMy-Ova mice, which express ovalbumin in the heart, caused a lethal myocarditis with 100% mortality by day 7, compared to zero mortality after transfer of the same number of control OT-I effectors. OT-I effectors generated in the absence of IL-12 do not infiltrate the myocardium, or induce myocarditis in cMy-mOva mice. CTLA-4-/- OT-I effectors generated without IL-12 do migrate into and damage the myocardium, albeit with delayed kinetics and reduced severity compared to CTLA-4-/- OT-I effectors generated with IL-12. These data show that CTLA-4 regulates pathogenic CD8+ T cell responses, and CTLA-4 deficiency partly overcomes a differentiation-block that exists when CD8+ T cells are stimulated without IL-12. Therefore, targeting CTLA-4 could influence effector CD8+ T cells in the setting of tumor therapy, autoimmunity and graft rejection.*
520 $a *This dissertation is a compound document (contains both a paper copy and a CD as part of the dissertation). The CD requires the following system requirements: Adobe Acrobat.
590 $a School code: 0084.
650 4 $a Biology, Cell. $3 1017686
650 4 $a Health Sciences, Immunology. $3 1017716
690 $a 0379
690 $a 0982
710 2 0 $a Harvard University. $3 528741
773 0 $t Dissertation Abstracts International $g 67-05B.
790 1 0 $a Lichtman, Andrew H., $e advisor
790 $a 0084
791 $a Ph.D.
792 $a 2006
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3217813