Such studies have shown that myeloid cells are required to induce the disease and IL-17-producing CD4(+) T cells may contribute to maintaining aldosterone-mediated hypertension.
Results showed that rs8193037 in IL17A was associated with the risk of congestive heart failure (odds ratio [OR] = 0.76; 95% confidence interval [CI] 0.63-0.90, adjusted P = 0.002) after adjustment for multiple cardiovascular risk factors including age, sex, smoking status, diabetes, hypertension, and dyslipidemia.
Due to its pleiotropic character, IL-17A is involved in the development of atherosclerosis, hypertension, diabetic nephropathy, ischaemia-reperfusion injury, fibrosis, glomerulonephritis, nephrotic syndrome, minimal change disease and acute renal allograft rejection.
We previously showed that angiotensin II (Ang II) increases T cell production of IL-17A, and that mice deficient in IL-17A have blunted hypertension and attenuated renal and vascular dysfunction.
It has been studied the function of CD68 and IL-17 in hypertension, but it has not been reported whether it affected hypertension and vascular remodeling when macrophage CD68 expression inhibited.
In additional experiments, we used a design to determine whether blockade of B7-dependent costimulation with CTLA4-Ig or blockade of IL-17 with IL-17-neutralizing antibody could prevent hypertension caused by faecal microbiota transplantation (FMT) from SHR to WKY.
Blood pressure increased after 14 days of IL-17A infusion in mice when compared with that in control mice, and this was associated to kidney infiltration by inflammatory cells, including CD3<sup>+</sup> and CD4<sup>+</sup> lymphocytes and neutrophils.