Table 1.

Therapeutic targets discussed in this review.

Type of Mediator	Description	Potential Application as a Target in Hypertension
Regulatory T-cells (Tregs)	T cell subtype characterized by the ability to suppress inflammatory signaling; proposed to be protective, where deficiency of Tregs leads to autoimmune disease	- Increasing the presence or  functionality of Tregs may reduce  oxidative stress, increase NO  bioavailability, block immune cell  accumulation, and protect  against hypertension
Th17 cells	T cell subtype that produces IL-17; pro-inflammatory and exacerbate tissue damage and disease	- Blunting Th17 signaling may  alleviate inflammation and target  organ tissue damage associated  with hypertension
Dendritic cells (DCs): - Classical DCs - Plasmacytoid DCs - Monocyte-derived inflammatory DCs - Langerhans cells	Bone marrow-derived antigen presenting cells (APCs) that play a key role in modulating the inflammatory response by distinguishing between self- and non-self antigens; induce the activation of T-lymphocytes	- Circulating precursor DCs as  biomarkers to predict the  development of cardiovascular  disease - Development of isoketal  scavengers to attenuate  immunogenicity of DCs and  hypertension
Immunosenescent CD8+ cells	T cells characterized by shortened telomeres, loss of CD28, gain of CD57 expression, and increased production of inflammatory cytokines and chemokines	- Biomarker and potential  therapeutic target in  hypertensive patients
Chemokines and cytokines - TNF-α - IL-17 - MCP-1 - IL-6 - CD40L	Activated and recruited immune cells produce these inflammatory mediators, which determine the local inflammatory response	- Implicated in development and  maintenance of hypertension - Blockade of these inflammatory  pathways may decrease  infiltration of immune cells,  inflammation and blood pressure
Toll-like receptors (TLRs: TLR1-13)	- Family of receptors that trigger pro-inflammatory signals in response to microbial structures or DAMPs released by injured tissues. - Potential molecular link between innate and adaptive immune responses in cardiovascular disease	- Targeting TLRs may modulate  the inflammatory cascade at an  earlier point to help control  disease more effectively
NLRP3 inflammasomes	- Pattern recognition receptors responsible for maturation of pro- inflammatory cytokines like IL-1β and IL-18 in response to PAMPs and DAMPs; - Controllers of the initiation of the  innate immune response	- Inflammasome inhibition has  been shown to prevent blood  pressure elevation, lower plasma  renin activity, and reduce sodium  retention - CIAS1 gene encoding for NLRP3  linked to essential hypertension  susceptibility