Leukocyte Bim deficiency does not impact atherogenesis in ldlr -/- mice, despite a pronounced induction of autoimmune inflammation

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dc.contributor.author Temmerman, Lieve
dc.contributor.author Westra, Marijke M.
dc.contributor.author Bot, Ilze
dc.contributor.author van Vlijmen, Bart J. M.
dc.contributor.author Van Bree, Niek
dc.contributor.author Bot, Martine
dc.contributor.author Habets, Kim L. L.
dc.contributor.author Keulers, Tom G. H.
dc.contributor.author van der Vlag, Johan
dc.contributor.author Cotter, Thomas G.
dc.contributor.author van Berkel, Theo J. C.
dc.contributor.author Biessen, Erik A. L.
dc.date.accessioned 2017-06-26T14:56:13Z
dc.date.available 2017-06-26T14:56:13Z
dc.date.issued 2017-06-08
dc.identifier.citation Temmerman, L., Westra, M. M., Bot, I., Vlijmen, B. J. M. v., Bree, N. V., Bot, M., Habets, K. L. L., Keulers, T. G. H., Vlag, J. v. d., Cotter, T. G., Berkel, T. J. C. v. and Biessen, E. A. L. (2017) 'Leukocyte Bim deficiency does not impact atherogenesis in ldlr −/− mice, despite a pronounced induction of autoimmune inflammation', Scientific Reports, 7(1), 3086. doi:10.1038/s41598-017-02771-4 en
dc.identifier.volume 7 en
dc.identifier.issued 1 en
dc.identifier.startpage 3086-1 en
dc.identifier.endpage 3086-11 en
dc.identifier.issn 2045-2322
dc.identifier.uri http://hdl.handle.net/10468/4190
dc.identifier.doi 10.1038/s41598-017-02771-4
dc.description.abstract Proapoptotic Bcl-2 family member Bim is particularly relevant for deletion of autoreactive and activated T and B cells, implicating Bim in autoimmunity. As atherosclerosis is a chronic inflammatory process with features of autoimmune disease, we investigated the impact of hematopoietic Bim deficiency on plaque formation and parameters of plaque stability. Bim−/− or wild type bone marrow transplanted ldlr−/− mice were fed a Western type diet (WTD) for 5 or 10 weeks, after which they were immunophenotyped and atherosclerotic lesions were analyzed. Bim−/− transplanted mice displayed splenomegaly and overt lymphocytosis. CD4+ and CD8+ T cells were more activated (increased CD69 and CD71 expression, increased interferon gamma production). B cells were elevated by 147%, with a shift towards the pro-atherogenic IgG-producing B2 cell phenotype, resulting in a doubling of anti-oxLDL IgG1 antibody titers in serum of bim−/− mice. Bim−/− mice displayed massive intraplaque accumulation of Ig complexes and of lesional T cells, although this did not translate in changes in plaque size or stability features (apoptotic cell and macrophage content). The surprising lack in plaque phenotype despite the profound pro-atherogenic immune effects may be attributable to the sharp reduction of serum cholesterol levels in WTD fed bim−/− mice. en
dc.format.mimetype application/pdf en
dc.language.iso en en
dc.publisher Nature Publishing Group en
dc.rights © The Authors 2017. Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit en
dc.rights.uri http://creativecommons.org/licenses/by/4.0/
dc.subject Atherosclerosis en
dc.subject Autoimmunity en
dc.subject Chronic inflammation en
dc.subject Experimental models of disease en
dc.title Leukocyte Bim deficiency does not impact atherogenesis in ldlr -/- mice, despite a pronounced induction of autoimmune inflammation en
dc.type Article (peer-reviewed) en
dc.internal.authorcontactother Thomas Cotter, School Of Biochemistry & Cell Biology, University College Cork, Cork, Ireland. +353-21-490-3000 Email: t.cotter@ucc.ie en
dc.internal.availability Full text available en
dc.date.updated 2017-06-26T14:52:01Z
dc.description.version Published Version en
dc.internal.rssid 400596065
dc.description.status Peer reviewed en
dc.identifier.journaltitle Scientific Reports en
dc.internal.copyrightchecked No !!CORA!! en
dc.internal.licenseacceptance Yes en
dc.internal.IRISemailaddress t.cotter@ucc.ie en
dc.identifier.articleid 3086


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© The Authors 2017. Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit Except where otherwise noted, this item's license is described as © The Authors 2017. Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit
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