000125631 001__ 125631
000125631 005__ 20240228143320.0
000125631 0247_ $$2doi$$a10.1371/journal.pone.0157311
000125631 0247_ $$2pmid$$apmid:27564380
000125631 0247_ $$2pmc$$apmc:PMC5001715
000125631 0247_ $$2altmetric$$aaltmetric:10862329
000125631 037__ $$aDKFZ-2017-01757
000125631 041__ $$aeng
000125631 082__ $$a500
000125631 1001_ $$aCheng, Fei$$b0
000125631 245__ $$aCombined B, T and NK Cell Deficiency Accelerates Atherosclerosis in BALB/c Mice.
000125631 260__ $$aLawrence, Kan.$$bPLoS$$c2016
000125631 3367_ $$2DRIVER$$aarticle
000125631 3367_ $$2DataCite$$aOutput Types/Journal article
000125631 3367_ $$0PUB:(DE-HGF)16$$2PUB:(DE-HGF)$$aJournal Article$$bjournal$$mjournal$$s1521118001_29643
000125631 3367_ $$2BibTeX$$aARTICLE
000125631 3367_ $$2ORCID$$aJOURNAL_ARTICLE
000125631 3367_ $$00$$2EndNote$$aJournal Article
000125631 520__ $$aThis study focused on the unique properties of both the Ldlr knockout defect (closely mimicking the human situation) and the BALB/c (C) inbred mouse strain (Th-2 slanted immune response). We generated two immunodeficient strains with severe combined B- and T-cell immunodeficiency with or without a complete lack of natural killer cells to revisit the role of adaptive immune responses on atherogenesis. C-Ldlr-/- Rag1-/- mice, which show severe combined B- and T-cell immunodeficiency and C-Ldlr-/- Rag1-/- Il2rg-/- mice, which combine the T- and B-cell defect with a complete lack of natural killer cells and inactivation of multiple cytokine signalling pathways were fed an atherogenic Western type diet (WTD). Both B6-Ldlr-/- and C-Ldlr-/- immunocompetent mice were used as controls. Body weights and serum cholesterol levels of both immunodeficient strains were significantly increased compared to C-Ldlr-/- controls, except for cholesterol levels of C-Ldlr-/- Rag1-/- double mutants after 12 weeks on the WTD. Quantification of the aortic sinus plaque area revealed that both strains of immunodeficient mice developed significantly more atherosclerosis compared to C-Ldlr-/- controls after 24 weeks on the WTD. Increased atherosclerotic lesion development in C-Ldlr-/- Rag1-/- Il2rg-/- triple mutants was associated with significantly increased numbers of macrophages and significantly decreased numbers of smooth muscle cells compared to both C-Ldlr-/- wild type and C-Ldlr-/- Rag1-/- double mutants pointing to a plaque destabilizing effect of NK cell loss. Collectively, the present study reveals a previously unappreciated complexity with regard to the impact of lymphocytes on lipoprotein metabolism and the role of lymphocyte subsets in plaque composition.
000125631 536__ $$0G:(DE-HGF)POF3-311$$a311 - Signalling pathways, cell and tumor biology (POF3-311)$$cPOF3-311$$fPOF III$$x0
000125631 588__ $$aDataset connected to CrossRef, PubMed,
000125631 650_7 $$2NLM Chemicals$$aLipoproteins
000125631 650_7 $$2NLM Chemicals$$aReceptors, LDL
000125631 650_7 $$2NLM Chemicals$$aTriglycerides
000125631 650_7 $$097C5T2UQ7J$$2NLM Chemicals$$aCholesterol
000125631 7001_ $$aTwardowski, Laura$$b1
000125631 7001_ $$0P:(DE-He78)ea7e63442b7f00c9561f7b959e237065$$aReifenberg, Kurt$$b2$$udkfz
000125631 7001_ $$aWinter, Kerstin$$b3
000125631 7001_ $$aCanisius, Antje$$b4
000125631 7001_ $$aPross, Eva$$b5
000125631 7001_ $$aFan, Jianglin$$b6
000125631 7001_ $$aSchmitt, Edgar$$b7
000125631 7001_ $$aShultz, Leonard D$$b8
000125631 7001_ $$aLackner, Karl J$$b9
000125631 7001_ $$aTorzewski, Michael$$b10
000125631 773__ $$0PERI:(DE-600)2267670-3$$a10.1371/journal.pone.0157311$$gVol. 11, no. 8, p. e0157311 -$$n8$$pe0157311 -$$tPLoS one$$v11$$x1932-6203$$y2016
000125631 909CO $$ooai:inrepo02.dkfz.de:125631$$pVDB
000125631 9101_ $$0I:(DE-588b)2036810-0$$6P:(DE-He78)ea7e63442b7f00c9561f7b959e237065$$aDeutsches Krebsforschungszentrum$$b2$$kDKFZ
000125631 9131_ $$0G:(DE-HGF)POF3-311$$1G:(DE-HGF)POF3-310$$2G:(DE-HGF)POF3-300$$3G:(DE-HGF)POF3$$4G:(DE-HGF)POF$$aDE-HGF$$bGesundheit$$lKrebsforschung$$vSignalling pathways, cell and tumor biology$$x0
000125631 9141_ $$y2016
000125631 915__ $$0StatID:(DE-HGF)0100$$2StatID$$aJCR$$bPLOS ONE : 2015
000125631 915__ $$0StatID:(DE-HGF)0200$$2StatID$$aDBCoverage$$bSCOPUS
000125631 915__ $$0StatID:(DE-HGF)0300$$2StatID$$aDBCoverage$$bMedline
000125631 915__ $$0StatID:(DE-HGF)0310$$2StatID$$aDBCoverage$$bNCBI Molecular Biology Database
000125631 915__ $$0StatID:(DE-HGF)0501$$2StatID$$aDBCoverage$$bDOAJ Seal
000125631 915__ $$0StatID:(DE-HGF)0500$$2StatID$$aDBCoverage$$bDOAJ
000125631 915__ $$0LIC:(DE-HGF)CCBYNV$$2V:(DE-HGF)$$aCreative Commons Attribution CC BY (No Version)$$bDOAJ
000125631 915__ $$0StatID:(DE-HGF)0600$$2StatID$$aDBCoverage$$bEbsco Academic Search
000125631 915__ $$0StatID:(DE-HGF)0030$$2StatID$$aPeer Review$$bASC
000125631 915__ $$0StatID:(DE-HGF)0199$$2StatID$$aDBCoverage$$bThomson Reuters Master Journal List
000125631 915__ $$0StatID:(DE-HGF)0111$$2StatID$$aWoS$$bScience Citation Index Expanded
000125631 915__ $$0StatID:(DE-HGF)0150$$2StatID$$aDBCoverage$$bWeb of Science Core Collection
000125631 915__ $$0StatID:(DE-HGF)1040$$2StatID$$aDBCoverage$$bZoological Record
000125631 915__ $$0StatID:(DE-HGF)1050$$2StatID$$aDBCoverage$$bBIOSIS Previews
000125631 915__ $$0StatID:(DE-HGF)9900$$2StatID$$aIF < 5
000125631 9201_ $$0I:(DE-He78)W410-20160331$$kW410$$lZentrum für Präklinische Forschung$$x0
000125631 980__ $$ajournal
000125631 980__ $$aVDB
000125631 980__ $$aI:(DE-He78)W410-20160331
000125631 980__ $$aUNRESTRICTED