Journal
ATHEROSCLEROSIS
Volume 267, Issue -, Pages 27-33Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.atherosclerosis.2017.10.026
Keywords
FOXP3 isoforms; Treg cells; Coronary artery disease; Alternative splicing
Funding
- Swedish Research Council [349-2007-8703]
- Swedish Heart-Lung Foundation
- Foundation for Strategic Research (SSF)
- Vinnova Foundation
- Stockholm County Council
- European Commission (project Athero-Flux)
- European Commission (project VIA)
- [06816]
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Background and aims: The expression of FOXP3 isoforms affects regulatory T (Treg) cell function. Reduced Treg cell function has been associated with coronary artery disease (CAD). However, alternative splicing of FOXP3 in CAD has not been investigated. Methods: FOXP3 splice variants and IL17A transcripts in peripheral blood mononuclear cells from stable CAD patients and healthy controls were quantified, and FOXP3 isoform expression in response to T cell receptor (TCR) stimulation or LDL was analyzed by flow cytometry. Results: Compared to healthy controls, CAD patients expressed significantly more FOXP3 transcripts that included exon 2, whereas alternative splicing of exon 7 in correlation with IL17A expression was reduced. Moreover, TCR stimulation, as well as exposure to LDL, decreased alternative splicing of FOXP3 in CD4+ T cells in vitro. Conclusions: Our results demonstrate that blood mononuclear cells in stable CAD patients express a ratio of FOXP3 isoforms that is characteristic for activated CD4+ T cells. (C) 2017 Elsevier B.V. All rights reserved.
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