Angiotensin II-Induced Memory γδ T Cells Sensitize Mice to a Mild Hypertensive Stimulus

Author:

Comeau Kevin1,Shokoples Brandon1,Caillon Antoine1,Paradis Pierre1ORCID,Schiffrin Ernesto L12ORCID

Affiliation:

1. Hypertension and Vascular Research Unit, Lady Davis Institute for Medical Research, McGill University , Montréal, Québec , Canada

2. Department of Medicine, Sir Mortimer B. Davis-Jewish General Hospital, McGill University , Montréal, Québec , Canada

Abstract

Abstract BACKGROUND Memory T cells develop during an initial hypertensive episode, sensitizing mice to develop hypertension from further mild hypertensive challenges. We hypothesized that memory γδ T cells develop after a hypertensive challenge and sensitize mice to develop hypertension in response to a subsequent mild hypertensive challenge. METHODS The first aim was to profile memory γδ T cells after a 14-day pressor dose angiotensin II (AngII) infusion (490 ng/kg/min, subcutaneously) in male mice. The second aim was to deplete γδ T cells during a second 14-day subpressor dose AngII challenge (140 ng/kg/min, subcutaneously) in mice pre-exposed to an initial pressor dose AngII challenge. The third aim was to transfer 2.5 × 105 live pre-activated or not γδ T cells from mice that had received a 14-day pressor dose AngII infusion or sham treatment, to naive recipient mice stimulated with a subpressor dose AngII infusion. RESULTS Effector memory γδ T cells increased 5.2-fold in mesenteric vessels and perivascular adipose tissue, and 1.8-fold in mesenteric lymph nodes in pressor dose AngII-infused mice compared with sham-treated mice. Mice depleted of γδ T cells had 14 mm Hg lower systolic blood pressure (SBP) elevation than control mice from day 7 to 14 of subpressor dose AngII infusion. Adoptive transfer of γδ T cells from hypertensive mice induced an 18 mm Hg higher SBP elevation compared with a subpressor dose AngII infusion vs. γδ T cells transferred from sham-treated mice. CONCLUSIONS Memory γδ T cells develop in response to hypertensive stimuli, and contribute to the pathogenesis of hypertension.

Funder

Canadian Institutes of Health Research

First Pilot Foundation

Canada Research Chair

Canada Fund for Innovation

McGill Department of Medicine Gordon Phillips Fellowship

Fonds de recherche Santé Québec

Lady Davis Institute

Publisher

Oxford University Press (OUP)

Subject

Internal Medicine

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