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Activation-induced FOXP3 isoform profile in peripheral CD4+T cells is associated with coronary artery disease
Linköping University, Department of Medical and Health Sciences, Division of Cardiovascular Medicine. Linköping University, Faculty of Medicine and Health Sciences.
Linköping University, Department of Medical and Health Sciences, Division of Cardiovascular Medicine. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Heart and Medicine Center, Department of Cardiology in Linköping.
Karolinska University Hospital, Sweden.
Karolinska University Hospital, Sweden.
2017 (English)In: Atherosclerosis, ISSN 0021-9150, E-ISSN 1879-1484, Vol. 267, p. 27-33Article in journal (Refereed) Published
Abstract [en]

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.

Place, publisher, year, edition, pages
ELSEVIER IRELAND LTD , 2017. Vol. 267, p. 27-33
Keywords [en]
FOXP3 isoforms; Treg cells; Coronary artery disease; Alternative splicing
National Category
Cell and Molecular Biology
Identifiers
URN: urn:nbn:se:liu:diva-143616DOI: 10.1016/j.atherosclerosis.2017.10.026ISI: 000416032800004PubMedID: 29100058OAI: oai:DiVA.org:liu-143616DiVA, id: diva2:1165622
Note

Funding Agencies|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]

Available from: 2017-12-13 Created: 2017-12-13 Last updated: 2018-01-13

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Lundberg, AnnaJonasson, Lena
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Division of Cardiovascular MedicineFaculty of Medicine and Health SciencesDepartment of Cardiology in Linköping
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