東華大學圖書館 |

Language: English

Help

回圖書館首頁

手機版館藏查詢

Back

Switch To: Labeled | MARC Mode | ISBD

The role of T-bet and eomesodermin i...

Intlekofer, Andrew Michael.

Linked to FindBook

Google Book

Amazon

博客來

The role of T-bet and eomesodermin in effector and memory CD8+ T cell differentiation.

Record Type:	Language materials, printed : Monograph/item
Title/Author:	The role of T-bet and eomesodermin in effector and memory CD8+ T cell differentiation./
Author:	Intlekofer, Andrew Michael.
Description:	146 p.
Notes:	Adviser: Steven L. Reiner.
Contained By:	Dissertation Abstracts International68-11B.
Subject:	Biology, General. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3292034
ISBN:	9780549346036

The role of T-bet and eomesodermin in effector and memory CD8+ T cell differentiation.
Intlekofer, Andrew Michael.

The role of T-bet and eomesodermin in effector and memory CD8+ T cell differentiation. - 146 p.

Adviser: Steven L. Reiner.

Thesis (Ph.D.)--University of Pennsylvania, 2007.

We sought to investigate the role of the T-box transcription factors, T-bet and eomesodermin (Eomes), in regulating the differentiation, homeostasis, and function of effector and memory CD8+ T cells. We found that T-bet and Eomes cooperatively control expression of genes required for cytotoxic effector function. CD8+ T cells deficient for both T-bet and Eomes fail to support host defense against lymphocytic choriomeningitis virus (LCMV) infection, lack the ability to kill target cells or secrete Type 1 cytokines, and undergo anomalous Type 17 differentiation. Upon infection with LCMV, mice with T cells lacking both T-bet and Eomes develop a CD8 + T cell-dependent, progressive wasting disease characterized by multi-organ neutrophilic inflammation. In addition to their essential role in effector differentiation, we found that T-bet and Eomes control the homeostasis of cytotoxic immune cells, as mice with compound mutations in the genes encoding T-bet and Eomes are nearly devoid of immune lineages dependent on interleukin 15 (IL-15), including memory CD8+ T cells. We determined that T-bet and Eomes are responsible for inducing enhanced expression of CD122, the receptor specifying IL-15 responsiveness. An examination of the differential contributions of T-bet and Eomes to CD8+ T cell differentiation revealed that T-bet preferentially drives terminal differentiation of effector-like cells at the expense of self-renewing memory cells. Thus, T-bet and Eomes appear to independently and semi-redundantly induce the genetic program necessary for Type 1 CD8+ T cell differentiation, whereas their unique functions may differentially contribute to acute versus long-term defense against intracellular pathogens.

ISBN: 9780549346036Subjects--Topical Terms:

1018625
Biology, General.

The role of T-bet and eomesodermin in effector and memory CD8+ T cell differentiation.
LDR:02641nam 2200289 a 45 001 943718
005 20110520
008 110520s2007 ||||||||||||||||| ||eng d
020 $a 9780549346036
035 $a (UMI)AAI3292034
035 $a AAI3292034
040 $a UMI $c UMI
100 1 $a Intlekofer, Andrew Michael. $3 1267756
245 1 4 $a The role of T-bet and eomesodermin in effector and memory CD8+ T cell differentiation.
300 $a 146 p.
500 $a Adviser: Steven L. Reiner.
500 $a Source: Dissertation Abstracts International, Volume: 68-11, Section: B, page: 7232.
502 $a Thesis (Ph.D.)--University of Pennsylvania, 2007.
520 $a We sought to investigate the role of the T-box transcription factors, T-bet and eomesodermin (Eomes), in regulating the differentiation, homeostasis, and function of effector and memory CD8+ T cells. We found that T-bet and Eomes cooperatively control expression of genes required for cytotoxic effector function. CD8+ T cells deficient for both T-bet and Eomes fail to support host defense against lymphocytic choriomeningitis virus (LCMV) infection, lack the ability to kill target cells or secrete Type 1 cytokines, and undergo anomalous Type 17 differentiation. Upon infection with LCMV, mice with T cells lacking both T-bet and Eomes develop a CD8 + T cell-dependent, progressive wasting disease characterized by multi-organ neutrophilic inflammation. In addition to their essential role in effector differentiation, we found that T-bet and Eomes control the homeostasis of cytotoxic immune cells, as mice with compound mutations in the genes encoding T-bet and Eomes are nearly devoid of immune lineages dependent on interleukin 15 (IL-15), including memory CD8+ T cells. We determined that T-bet and Eomes are responsible for inducing enhanced expression of CD122, the receptor specifying IL-15 responsiveness. An examination of the differential contributions of T-bet and Eomes to CD8+ T cell differentiation revealed that T-bet preferentially drives terminal differentiation of effector-like cells at the expense of self-renewing memory cells. Thus, T-bet and Eomes appear to independently and semi-redundantly induce the genetic program necessary for Type 1 CD8+ T cell differentiation, whereas their unique functions may differentially contribute to acute versus long-term defense against intracellular pathogens.
590 $a School code: 0175.
650 4 $a Biology, General. $3 1018625
650 4 $a Biology, Molecular. $3 1017719
650 4 $a Health Sciences, Immunology. $3 1017716
690 $a 0306
690 $a 0307
690 $a 0982
710 2 $a University of Pennsylvania. $3 1017401
773 0 $t Dissertation Abstracts International $g 68-11B.
790 $a 0175
790 1 0 $a Reiner, Steven L., $e advisor
791 $a Ph.D.
792 $a 2007
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3292034