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Novel roles for NFAT in T and B cell...

Borde, Madhuri.

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Novel roles for NFAT in T and B cell tolerance.

Record Type:	Electronic resources : Monograph/item
Title/Author:	Novel roles for NFAT in T and B cell tolerance./
Author:	Borde, Madhuri.
Description:	150 p.
Notes:	Source: Dissertation Abstracts International, Volume: 67-02, Section: B, page: 0697.
Contained By:	Dissertation Abstracts International67-02B.
Subject:	Biology, Molecular. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3205891
ISBN:	9780542544415

Novel roles for NFAT in T and B cell tolerance.
Borde, Madhuri.

Novel roles for NFAT in T and B cell tolerance. - 150 p.

Source: Dissertation Abstracts International, Volume: 67-02, Section: B, page: 0697.

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

While somatic recombination of antigen receptors allows for a diverse repertoire of antigen-specific lymphocytes, it can also lead to the production of T and B cells that are autoreactive. As a consequence, central and peripheral tolerance have evolved to protect against lymphocytes harboring the potential to become activated by self-antigen. Cell-intrinsic anergy and dominant tolerance mediated by CD4+CD25+ regulatory T cells constitute two important modes of peripheral tolerance.

ISBN: 9780542544415Subjects--Topical Terms:

1017719
Biology, Molecular.

Novel roles for NFAT in T and B cell tolerance.
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100 1 $a Borde, Madhuri. $3 1917870
245 1 0 $a Novel roles for NFAT in T and B cell tolerance.
300 $a 150 p.
500 $a Source: Dissertation Abstracts International, Volume: 67-02, Section: B, page: 0697.
500 $a Adviser: Anjana Rao.
502 $a Thesis (Ph.D.)--Harvard University, 2006.
520 $a While somatic recombination of antigen receptors allows for a diverse repertoire of antigen-specific lymphocytes, it can also lead to the production of T and B cells that are autoreactive. As a consequence, central and peripheral tolerance have evolved to protect against lymphocytes harboring the potential to become activated by self-antigen. Cell-intrinsic anergy and dominant tolerance mediated by CD4+CD25+ regulatory T cells constitute two important modes of peripheral tolerance.
520 $a Low level stimulation of B cells by self-antigen results in elevated basal intracellular calcium concentrations and subsequent activation of Erk and NFAT signaling pathways. Previous work from the lab has shown that sustained calcium signaling in T cells, which activates NFAT in the absence of NF-&square;B or AP-1, diverts the transcription factor NFAT to transcribing a set of genes that encode a variety of known or putative negative regulators of TCR signaling. We have suggested that cell-intrinsic T cell anergy/tolerance is imposed, at least in part, through the calcium/calcineurin/NFAT pathway via induction of a negative regulatory gene expression program.
520 $a We hypothesized that the preferential activation of NFAT in tolerant B cells could induce the transcription of anergy-related genes in B cells, in a manner analogous to its function in T cell anergy. In order to test whether the low-level activation of NFAT contributed to B cell anergy, we evaluated the requirement for NFAT1 in a well-established model of B cell tolerance, the MD4/sHEL double transgenic mouse model. The loss of NFAT1 allowed the aberrant accumulation of mature tolerant B cells and production of antibodies upon stimulation with self antigen in the presence of T cell help, demonstrating that the transcription factor NFAT1 has a role in the induction and/or maintenance of B cell tolerance.
520 $a The dominant tolerance mediated by regulatory T cells (Treg) constitutes a critical component of peripheral tolerance. When co-cultured with effector T cells and stimulated in vitro, regulatory T cells can suppress the ability of the effector T cells to produce IL-2 and proliferate. FOXP3 is the major transcriptional regulator controlling differentiation of thymic-derived Tregs. T cells transduced with Foxp3 acquire many phenotypic and functional characteristics of thymic-derived Tregs. The molecular mechanisms by which FOXP3 induces these changes in unknown; although a mechanism involving displacement of NFAT from NFAT:AP-1 sites has been postulated. (Abstract shortened by UMI.)
590 $a School code: 0084.
650 4 $a Biology, Molecular. $3 1017719
650 4 $a Biology, Cell. $3 1017686
650 4 $a Health Sciences, Immunology. $3 1017716
690 $a 0307
690 $a 0379
690 $a 0982
710 2 0 $a Harvard University. $3 528741
773 0 $t Dissertation Abstracts International $g 67-02B.
790 1 0 $a Rao, Anjana, $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=3205891