Table 1.

Examples of inflammatory cytokines involved in hypertension.

Cytokines	Cell sources	Disease models	Mechanisms	Biological effects	Reference
IL-17	CD4+ T cells and some CD8+ cells	IL-17A-/- mice	Enhance CCL-2 in an NADPH oxidase-dependent manner, and altering gene expression in vascular smooth muscle cells	Promotes oxidative stress and increases the number of infiltrated T cells	(70–72)
IL-6	Monocytes, macrophages, dendritic cells, etc.	IL-6-/- mice	polarizes the CD4+ cells and facilitates water and sodium retention	promotes the production of IL-17 and upregulates the expression and increase the activity of the epithelial sodium channel in duct cells	(73–75)
TNF-α	Monocytes and macrophages	rheumatoid arthritis patients	NF-κB and NADPH oxidase activation	upregulates the expressions of chemokine and adhesion molecule in vessels, facilitates microvascular remodeling and sodium retention, and reduce NO production	(76–81)
IFN-γ	Th1 cells	Ang II-treated IFN-γR knockout mice	Increases the angiotensinogen expression	Promotes renal fibrosis and decreases glomerular filtration rate	(82)
IL-1β	Monocytes, T cells and neutrophils	Diabetic db/db mice	Polarize the naïve macrophages into M1 subtype	Releases a large amount of IL-6	(83)

CCL-2, C-C motif chemokine ligand 2; IL, interleukin; IFN-γ, interferon gamma; NADPH, nicotinamide adenine dinucleotide phosphate; NF-κB, nuclear factor kappa-B; NO, nitric oxide; Th, T helper; TNF-α, tumor necrosis factor α.