TAP1-Deficiency Does Not Alter Atherosclerosis Development in Apoe−/− Mice

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TAP1-Deficiency Does Not Alter Atherosclerosis Development in Apoe−/− Mice

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Publication Article, peer reviewed scientific
Title TAP1-Deficiency Does Not Alter Atherosclerosis Development in Apoe−/− Mice
Author(s) Kolbus, Daniel ; Ljungcrantz, Irena ; Söderberg, Ingrid ; Alm, Ragnar ; Björkbacka, Harry ; Nilsson, Jan ; Nordin Fredrikson, Gunilla
Date 2012
English abstract
Antigen presenting cells (APC) have the ability to present both extra-cellular and intra-cellular antigens via MHC class I molecules to CD8+ T cells. The cross presentation of extra-cellular antigens is reduced in mice with deficient Antigen Peptide Transporter 1 (TAP1)-dependent MHC class I antigen presentation, and these mice are characterized by a diminished CD8+ T cell population. We have recently reported an increased activation of CD8+ T cells in hypercholesterolemic Apoe−/− mice. Therefore, this study included TAP1-deficient Apoe−/− mice (Apoe−/−Tap1−/−) to test the atherogenicity of CD8+ T cells and TAP1-dependent cross presentation in a hypercholesterolemic environment. As expected the CD8+ T cell numbers were low in Apoe−/−Tap1−/− mice in comparison to Apoe−/− mice, constituting ~1% of the lymphocyte population. In spite of this there were no differences in the extent of atherosclerosis as assessed by en face Oil Red O staining of the aorta and cross-sections of the aortic root between Apoe−/−Tap1−/− and Apoe−/− mice. Moreover, no differences were detected in lesion infiltration of macrophages or CD3+ T cells in Apoe−/−Tap1−/− compared to Apoe−/− mice. The CD3+CD4+ T cell fraction was increased in Apoe−/−Tap1−/− mice, suggesting a compensation for the decreased CD8+ T cell population. Interestingly, the fraction of CD8+ effector memory T cells was increased but this appeared to have little impact on the atherosclerosis development. In conclusion, Apoe−/−Tap1−/− mice develop atherosclerosis equal to Apoe−/− mice, indicating a minor role for CD8+ T cells and TAP1-dependent antigen presentation in the disease process.
DOI http://dx.doi.org/10.1371/journal.pone.0033932 (link to publisher's fulltext)
Publisher Public Library of Science
Host/Issue PLOS One;7
Volume 3
ISSN 1932-6203
Pages e33932
Language eng (iso)
Subject(s) Medicine
Research Subject Categories::MEDICINE
Handle http://hdl.handle.net/2043/15973 (link to this page)

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