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Toll-like receptor function and sign...

Gelman, Andrew E.

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Toll-like receptor function and signaling pathways in CD4+ T cells.

Record Type:	Electronic resources : Monograph/item
Title/Author:	Toll-like receptor function and signaling pathways in CD4+ T cells./
Author:	Gelman, Andrew E.
Description:	76 p.
Notes:	Source: Dissertation Abstracts International, Volume: 67-07, Section: B, page: 3688.
Contained By:	Dissertation Abstracts International67-07B.
Subject:	Biology, Cell. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3225461
ISBN:	9780542798962

Toll-like receptor function and signaling pathways in CD4+ T cells.
Gelman, Andrew E.

Toll-like receptor function and signaling pathways in CD4+ T cells. - 76 p.

Source: Dissertation Abstracts International, Volume: 67-07, Section: B, page: 3688.

Thesis (Ph.D.)--University of Pennsylvania, 2006.

The functional significance of toll-like receptor (TLR) expression on T cells is not clear. Here I show that activated CD4+ T cells enhance their survival in response to direct stimulation by either the TLR3 agonist Poly I:C or the TLR9 agonist CpG DNA. TLR agonist mediated survival of activated CD4+ T cells is dependent on NF-kappaB activation and is associated with Bcl-xL upregulation. CpG DNA can also act as a comitogen for CD4+ T cells by enhancing IL-2 production and preventing anergy via a MyD88 and PI-3 kinase dependent pathway. PI-3 kinase activation requires a putative SH2-binding motif in the MyD88 TIR domain, as reconstitution of MyD88-deficient primary CD4+ T cells with a mutated MyD88 transgene abrogated association of PI-3 kinase with MyD88, phosphorylation of Akt and GSK-3, and IL-2 production. In contrast, the MyD88 death domain is required for NF-kappaB activation and survival. These studies identify a novel MyD88-dependent PI-3 kinase signaling pathway in T cells that differentiates CpG DNA mediated proliferation from survival.

ISBN: 9780542798962Subjects--Topical Terms:

1017686
Biology, Cell.

Toll-like receptor function and signaling pathways in CD4+ T cells.
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245 1 0 $a Toll-like receptor function and signaling pathways in CD4+ T cells.
300 $a 76 p.
500 $a Source: Dissertation Abstracts International, Volume: 67-07, Section: B, page: 3688.
500 $a Adviser: Laurence A. Turka.
502 $a Thesis (Ph.D.)--University of Pennsylvania, 2006.
520 $a The functional significance of toll-like receptor (TLR) expression on T cells is not clear. Here I show that activated CD4+ T cells enhance their survival in response to direct stimulation by either the TLR3 agonist Poly I:C or the TLR9 agonist CpG DNA. TLR agonist mediated survival of activated CD4+ T cells is dependent on NF-kappaB activation and is associated with Bcl-xL upregulation. CpG DNA can also act as a comitogen for CD4+ T cells by enhancing IL-2 production and preventing anergy via a MyD88 and PI-3 kinase dependent pathway. PI-3 kinase activation requires a putative SH2-binding motif in the MyD88 TIR domain, as reconstitution of MyD88-deficient primary CD4+ T cells with a mutated MyD88 transgene abrogated association of PI-3 kinase with MyD88, phosphorylation of Akt and GSK-3, and IL-2 production. In contrast, the MyD88 death domain is required for NF-kappaB activation and survival. These studies identify a novel MyD88-dependent PI-3 kinase signaling pathway in T cells that differentiates CpG DNA mediated proliferation from survival.
590 $a School code: 0175.
650 4 $a Biology, Cell. $3 1017686
650 4 $a Health Sciences, Immunology. $3 1017716
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773 0 $t Dissertation Abstracts International $g 67-07B.
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