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Autophagy, ROS and aging impact cyto...

Tal, Michal Caspi.

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Autophagy, ROS and aging impact cytosolic antiviral immunity.

Record Type:	Language materials, printed : Monograph/item
Title/Author:	Autophagy, ROS and aging impact cytosolic antiviral immunity./
Author:	Tal, Michal Caspi.
Description:	179 p.
Notes:	Source: Dissertation Abstracts International, Volume: 74-05(E), Section: B.
Contained By:	Dissertation Abstracts International74-05B(E).
Subject:	Health Sciences, Immunology. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3535395
ISBN:	9781267856753

Autophagy, ROS and aging impact cytosolic antiviral immunity.
Tal, Michal Caspi.

Autophagy, ROS and aging impact cytosolic antiviral immunity. - 179 p.

Source: Dissertation Abstracts International, Volume: 74-05(E), Section: B.

Thesis (Ph.D.)--Yale University, 2012.

In this thesis we show that pro-inflammatory cytokine production in response to viral ligands is increased in several situations: (1) in the absence of autophagy, (2) during increased oxidative stress, and (3) in the elderly. We find that autophagy is essential for maintaining the integrity of, and the appropriate amount of, mitochondria. Mitochondria serve as an integral platform whereby antiviral defense initiation pathways are coordinated with sensing of cellular stress, and thereby autophagy is critical for regulating the signaling emanating from the mitochondria. Accumulation of damaged mitochondria within a cell leads to increased mitochondrial reactive oxygen species production, and our studies show that this leads in increased cytosolic antiviral signaling and confers some protection from viral infection. Further, we find evidence for defective autophagy in human aging, as well as increased levels of mitochondrial ROS with age. We find this even in hematopoietic stem cells and throughout the progeny hematopoietic cells and we investigate the functional implications for the accumulation of damaged mitochondria and elevated levels of oxidative stress on the innate immune response to viral infection in the elderly. The implications of this study are that modulation of autophagy levels or the dysregulated pro-inflammatory cytokine production that results from defects in autophagy could possibly benefit the aging antiviral immune response.

ISBN: 9781267856753Subjects--Topical Terms:

1017716
Health Sciences, Immunology.

Autophagy, ROS and aging impact cytosolic antiviral immunity.
LDR:02335nam a2200289 4500 001 1968974
005 20141219110805.5
008 150210s2012 ||||||||||||||||| ||eng d
020 $a 9781267856753
035 $a (MiAaPQ)AAI3535395
035 $a AAI3535395
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100 1 $a Tal, Michal Caspi. $3 2106216
245 1 0 $a Autophagy, ROS and aging impact cytosolic antiviral immunity.
300 $a 179 p.
500 $a Source: Dissertation Abstracts International, Volume: 74-05(E), Section: B.
500 $a Adviser: Akiko Iwasaki.
502 $a Thesis (Ph.D.)--Yale University, 2012.
520 $a In this thesis we show that pro-inflammatory cytokine production in response to viral ligands is increased in several situations: (1) in the absence of autophagy, (2) during increased oxidative stress, and (3) in the elderly. We find that autophagy is essential for maintaining the integrity of, and the appropriate amount of, mitochondria. Mitochondria serve as an integral platform whereby antiviral defense initiation pathways are coordinated with sensing of cellular stress, and thereby autophagy is critical for regulating the signaling emanating from the mitochondria. Accumulation of damaged mitochondria within a cell leads to increased mitochondrial reactive oxygen species production, and our studies show that this leads in increased cytosolic antiviral signaling and confers some protection from viral infection. Further, we find evidence for defective autophagy in human aging, as well as increased levels of mitochondrial ROS with age. We find this even in hematopoietic stem cells and throughout the progeny hematopoietic cells and we investigate the functional implications for the accumulation of damaged mitochondria and elevated levels of oxidative stress on the innate immune response to viral infection in the elderly. The implications of this study are that modulation of autophagy levels or the dysregulated pro-inflammatory cytokine production that results from defects in autophagy could possibly benefit the aging antiviral immune response.
590 $a School code: 0265.
650 4 $a Health Sciences, Immunology. $3 1017716
650 4 $a Health Sciences, Aging. $3 1669845
650 4 $a Biology, Virology. $3 1019068
690 $a 0982
690 $a 0493
690 $a 0720
710 2 $a Yale University. $b Immunobiology. $3 2101670
773 0 $t Dissertation Abstracts International $g 74-05B(E).
790 $a 0265
791 $a Ph.D.
792 $a 2012
793 $a English
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3535395