Infiltrating T helper 17 cells in the paraventricular nucleus are pathogenic for stress-induced hypertension.

Central neuroinflammation produced by both innate and adaptive immunities plays a major role in the development of stress-induced hypertension (SIH), but successful T cell immunoregulation for SIH requires that the T cells can access brain tissues. So far, both the effects of T helper 17 (Th17) cells on SIH and the pathway for T cells entry into the brain were unknown. Here we show that the blood pressure (BP), heart rate (HR) and the norepinephrine(NE) of the SIH rats were considerably higher, the numbers of Th17 cells and IL-17 were higher, relative to control. Anti-IL-17 attenuated the elevation of BP and HR of the SIH rats when microinjected into the paraventricular nucleus (PVN).Alb-FITC, after infusion into the carotid artery, were found in the brain parenchyma of the PVN in the SIH rats. We concluded that Th17 cells infiltrated the parenchyma of the paraventricular nucleus (PVN) via a compromised blood brain barrier (BBB) in response to stress and Th17 cells and IL-17 play an important role in the pathophysiology of SIH. • The permeability of BBB increased and Th17 cells infiltrate into brain parenchyma in the PVN of SIH rats. • ROR-γt or CD4 and IL-17 co-existin the paraventricular hypothalamic nucleus and expression of IL-17, CD4 or ROR-γt increased. • Microinjection of Anti-IL-17 in the PVN reduced the serum NE concentration and decreased systolic blood pressure of SIH rats. [ABSTRACT FROM AUTHOR]