A deficiency in the in vivo clearance of apopototic cells is a feature of the NOD mouse

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dc.contributor.author O'Brien, B
dc.contributor.author Geng, X
dc.contributor.author Orteu, CH
dc.contributor.author Huang, Y
dc.contributor.author Ghoreishi, M
dc.contributor.author Zhang, Y
dc.contributor.author Bush, JA
dc.contributor.author Li, G
dc.contributor.author Finegood, DT
dc.contributor.author Dutz, JP
dc.date.accessioned 2009-12-21T02:34:54Z
dc.date.issued 2006-01
dc.identifier.citation Journal of Autoimmunity, 2006, 26 (2), pp. 104 - 115
dc.identifier.issn 0896-8411
dc.identifier.other C1 en_US
dc.identifier.uri http://hdl.handle.net/10453/4820
dc.description.abstract Deficiencies in apoptotic cell clearance have been linked to autoimmunity. Here we examined the time-course of peritoneal macrophage phagocytosis of dying cells following the direct injection of apoptotic thymocytes into the peritoneum of NOD mice and BALB/c controls. Macrophages from NOD mice demonstrated a profound defect in the phagocytosis of apoptotic thymocytes as compared to control macrophages. Nonobese diabetic mice also demonstrated a decrease in the clearance of apoptotic cell loads following an apoptotic stimulus to thymocytes (dexamethasone) when compared to BALB/c or NOR controls. Further, NOD mice demonstrated an increase in apoptotic cell load following an apoptotic stimulus to keratinocytes (ultraviolet light, UVB) when compared to control strains. Animals deficient in macrophage phagocytosis of apoptotic debris often manifest an autoimmune phenotype characterized by the production of antinuclear autoantibodies (ANA). We determined whether increased apoptotic cell loads (through repeated exposure to UVB irradiation) could accelerate such autoimmune phenomena in young NOD mice. Following repeated UVB irradiation, NOD mice, but not BALB/c or NOR controls, developed ANA. We propose that abnormalities in apoptotic cell clearance by macrophages predispose NOD mice to autoimmunity.
dc.publisher Academic Press
dc.relation.isbasedon 10.1016/j.jaut.2005.11.006
dc.title A deficiency in the in vivo clearance of apopototic cells is a feature of the NOD mouse
dc.type Journal Article
dc.parent Journal of Autoimmunity
dc.journal.volume 2
dc.journal.volume 26
dc.journal.number en_US
dc.journal.number 2 en_US
dc.publocation United Kingdom en_US
dc.identifier.startpage en_US
dc.identifier.startpage 104 en_US
dc.identifier.endpage en_US
dc.identifier.endpage 115 en_US
dc.cauo.name SCI.Medical and Molecular Biosciences en_US
dc.conference Verified OK en_US
dc.for 1107 Immunology
dc.personcode 030027
dc.percentage 100 en_US
dc.classification.name Biochemistry and Cell Biology en_US
dc.classification.type FOR-08 en_US
dc.description.keywords clearance
dc.description.keywords macrophages
dc.description.keywords autoimmunity
dc.description.keywords diabetes
dc.description.keywords apoptosis
pubs.embargo.period Not known
pubs.organisational-group /University of Technology Sydney
pubs.organisational-group /University of Technology Sydney/Faculty of Science
pubs.organisational-group /University of Technology Sydney/Strength - Health Technologies
utslib.copyright.status Closed Access
utslib.copyright.date 2015-04-15 12:17:09.805752+10
pubs.consider-herdc true
utslib.collection.history Closed (ID: 3)
utslib.collection.history School of Medical and Molecular Sciences (ID: 341)


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