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Regulation of Fc receptor expression...

Chong, Hey Jin.

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Regulation of Fc receptor expression and signaling on murine mast cells.

Record Type:	Electronic resources : Monograph/item
Title/Author:	Regulation of Fc receptor expression and signaling on murine mast cells./
Author:	Chong, Hey Jin.
Description:	171 p.
Notes:	Source: Dissertation Abstracts International, Volume: 65-01, Section: B, page: 0145.
Contained By:	Dissertation Abstracts International65-01B.
Subject:	Health Sciences, Immunology. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3118821
ISBN:	0496662430

Regulation of Fc receptor expression and signaling on murine mast cells.
Chong, Hey Jin.

Regulation of Fc receptor expression and signaling on murine mast cells. - 171 p.

Source: Dissertation Abstracts International, Volume: 65-01, Section: B, page: 0145.

Thesis (Ph.D.)--Virginia Commonwealth University, 2004.

Mast cells have long been appreciated as the primary effector cells in allergy and asthma, and recently have been implicated in other inflammatory diseases. Using high density oligonucleotide probe arrays, we assessed genome-wide transcriptional profiles after FcepsilonRI aggregation for 90 minutes, 5 hours and 24 hours. We describe novel gene regulation in response to FcepsilonRI signaling, including altered expression of CD44, Par1, osteopontin, Nur77, E4BP4, and NDRG1. In addition, the gene encoding FcepsilonRI beta was downregulated 5 hours after mast cell activation according to both microarray analysis and RPA, and western blotting confirmed the downregulation of the beta subunit protein. Moreover, this downregulation of beta mRNA correlated with the decreased FCepsilonRI surface expression after mast cell activation. Very little is known about the transcriptional regulation of the beta subunit of FcepsilonRI. These transcriptome profiling experiments are revealing novel and clinically relevant insight into how FcepsilonRI signaling may be controlled.

ISBN: 0496662430Subjects--Topical Terms:

1017716
Health Sciences, Immunology.

Regulation of Fc receptor expression and signaling on murine mast cells.
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100 1 $a Chong, Hey Jin. $3 1939119
245 1 0 $a Regulation of Fc receptor expression and signaling on murine mast cells.
300 $a 171 p.
500 $a Source: Dissertation Abstracts International, Volume: 65-01, Section: B, page: 0145.
500 $a Director: John Joseph Ryan.
502 $a Thesis (Ph.D.)--Virginia Commonwealth University, 2004.
520 $a Mast cells have long been appreciated as the primary effector cells in allergy and asthma, and recently have been implicated in other inflammatory diseases. Using high density oligonucleotide probe arrays, we assessed genome-wide transcriptional profiles after FcepsilonRI aggregation for 90 minutes, 5 hours and 24 hours. We describe novel gene regulation in response to FcepsilonRI signaling, including altered expression of CD44, Par1, osteopontin, Nur77, E4BP4, and NDRG1. In addition, the gene encoding FcepsilonRI beta was downregulated 5 hours after mast cell activation according to both microarray analysis and RPA, and western blotting confirmed the downregulation of the beta subunit protein. Moreover, this downregulation of beta mRNA correlated with the decreased FCepsilonRI surface expression after mast cell activation. Very little is known about the transcriptional regulation of the beta subunit of FcepsilonRI. These transcriptome profiling experiments are revealing novel and clinically relevant insight into how FcepsilonRI signaling may be controlled.
520 $a Continuing with our focus on how mast cell activation is regulated, we examined the effects of Th2 cytokines on expression of important surface receptors. Murine mast cells co-express the activation receptor FcgammaRIII and the inhibitory receptor FcgammaIIb and can be activated by IgG immune complexes. Using mouse bone marrow-derived mast cells, we report that IL-4 selectively increases FcgammaRIII expression without altering FcgammaRIIb. This enhanced expression could be induced by Stat6 activation alone, and appeared to be mediated in part by increased FcgammaRIIIalpha protein synthesis without significant changes in transcription. The increase in FcgammaRIII expression was functionally significant, as it was matched by enhanced FcgammaR-mediated degranulation and cytokine production. Selective regulation of mast cell FcgammaR by IL-4 could alter inflammatory IgG responses and subsequently disease severity and progression. Collectively, our studies have used genome-wide screening and reductionist studies to demonstrate mechanisms by which mast cell function is regulated.
590 $a School code: 2383.
650 4 $a Health Sciences, Immunology. $3 1017716
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710 2 0 $a Virginia Commonwealth University. $3 1018010
773 0 $t Dissertation Abstracts International $g 65-01B.
790 1 0 $a Ryan, John Joseph, $e advisor
790 $a 2383
791 $a Ph.D.
792 $a 2004
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3118821