Abstract

The immune system plays a critical role in hypertension progression. It has been showed that the lack of T cells prevented the development of hypertension. However, the role of myeloid cells in this process is elusive. We now show that there is a 2 fold increase of CD11b+ Gr1+ myeloid cells in murine hypertension models induced by angiotensin II, L-NAME or high salt diet. These increased myeloid cells are immunosuppressive in that they could suppress T cell proliferation. The production of reactive oxygen species mediates their immunosuppressive functions. When hypertensive mice were depleted of these myeloid cells, using either anti-Gr1 antibody or gemcitabine, there was a 15 mmHg further rise in blood pressure and aggravation of T cell activation as manifested by increased production of IFN-γ, TNFα and IL-17 in both spleen and kidney. In contrast, adoptive transfer of myeloid-derived suppressor cells could be used as both treatment reagent to alleviate established hypertension and preventive reagent from hypertensive insult. These data unveil the role of a distinctive myeloid population in hypertension, which may be a potential target for hypertension management.

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