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Blood pressure regulation by CD4lymphocytes expressing choline acetyltransferase
Center for Bioelectronic Medicine, Department of Medicine, Center for Molecular Medicine, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden / Laboratory of Biomedical Science, The Feinstein Institute for Medical Research, Manhasset, New York, USA.
Laboratory of Biomedical Science, The Feinstein Institute for Medical Research, Manhasset, New York, USA / The Campbell Family Institute for Breast Cancer Research, University Health Network, Toronto, Ontario, Canada.
Division of Cardiology, Peter Munk Cardiac Centre, University Health Network, Toronto, Ontario, Canada.
The Campbell Family Institute for Breast Cancer Research, University Health Network, Toronto, Ontario, Canada.
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2016 (engelsk)Inngår i: Nature Biotechnology, ISSN 1087-0156, E-ISSN 1546-1696, Vol. 34, nr 10, s. 1066-1071Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Blood pressure regulation is known to be maintained by a neuro-endocrine circuit, but whether immune cells contribute to blood pressure homeostasis has not been determined. We previously showed that CD4(+) T lymphocytes that express choline acetyltransferase (ChAT), which catalyzes the synthesis of the vasorelaxant acetylcholine, relay neural signals(1). Here we show that these CD4(+)CD44(hi)CD62L(Io) T helper cells by gene expression are a distinct T-cell population defined by ChAT (CD4 T-ChAT). Mice lacking ChAT expression in CD4(+) cells have elevated arterial blood pressure, compared to littermate controls. Jurkat T cells overexpressing ChAT (JT(ChAT)) decreased blood pressure when infused into mice. Co-incubation of JT(ChAT) and endothelial cells increased endothelial cell levels of phosphorylated endothelial nitric oxide synthase, and of nitrates and nitrites in conditioned media, indicating increased release of the potent vasorelaxant nitric oxide. The isolation and characterization of CD4 T-ChAT cells will enable analysis of the role of these cells in hypotension and hypertension, and may suggest novel therapeutic strategies by targeting cell-mediated vasorelaxation.

sted, utgiver, år, opplag, sider
Nature Publishing Group, 2016. Vol. 34, nr 10, s. 1066-1071
Emneord [en]
CD4-positive T cells, Experimental models of disease, Hypertension, Mechanisms of disease, Neuro–vascular interactions
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URN: urn:nbn:se:his:diva-13115DOI: 10.1038/nbt.3663ISI: 000386317500022PubMedID: 27617738Scopus ID: 2-s2.0-84991581707OAI: oai:DiVA.org:his-13115DiVA, id: diva2:1048249
Tilgjengelig fra: 2016-11-21 Laget: 2016-11-18 Sist oppdatert: 2018-01-13bibliografisk kontrollert

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