title: Immunity in arterial hypertension: associations or causalities?
abstract: Numerous studies describe associations between markers of inflammation and arterial hypertension (aHT), but does that imply causality? Interventional studies that reduce blood pressure reduced also markers of inflammation, but does immunosuppression improve hypertension? Here, we review the available mechanistic data. Aberrant immunity can trigger endothelial dysfunction but is hardly ever the primary cause of aHT. Innate and adaptive immunity get involved once hypertension has caused vascular wall injury as immunity is a modifier of endothelial dysfunction and vascular wall remodelling. As vascular remodelling progresses, immunity-related mechanisms can become significant cofactors for cardiovascular (CV) disease progression; vice versa, suppressing immunity can improve hypertension and CV outcomes. Innate and adaptive immunity both contribute to vascular wall remodelling. Innate immunity is driven by danger signals that activate Toll-like receptors and other pattern-recognition receptors. Adaptive immunity is based on loss of tolerance against vascular autoantigens and includes autoreactive T-cell immunity as well as non-HLA angiotensin II type 1 receptor-activating autoantibodies. Such processes involve numerous other modulators such as regulatory T cells. Together, immunity is not causal for hypertension but rather an important secondary pathomechanism and a potential therapeutic target in hypertension.
authors.affiliation: Nephrologisches Zentrum, Medizinische Klinik und Poliklinik IV, Klinikum der Universität München, Munich, Germany.
authors.forename: Hans-Joachim
authors.initials: HJ
authors.lastname: Anders
authors.affiliation: Department of Nephrology, Klinikum rechts der Isar der Technischen Universität München, Munich, Germany.
authors.forename: Marcus
authors.initials: M
authors.lastname: Baumann
authors.affiliation: Nephrology, Dialysis and Transplantation Unit & CNR-IFC, Clinical Epidemiology and Physiopathology of Renal Disease and Hypertension of Reggio Calabria, Reggio Calabria, Italy.
authors.forename: Giovanni
authors.initials: G
authors.lastname: Tripepi
authors.affiliation: Nephrology, Dialysis and Transplantation Unit & CNR-IFC, Clinical Epidemiology and Physiopathology of Renal Disease and Hypertension of Reggio Calabria, Reggio Calabria, Italy.
authors.forename: Francesca
authors.initials: F
authors.lastname: Mallamaci
mesh_terms: D000818:Animals; D002318:Cardiovascular Diseases / Q000150:complications* / Q000276:immunology; D015984:Causality; D006801:Humans; D006973:Hypertension / Q000209:etiology*; D007113:Immunity, Innate / Q000276:immunology*; D007249:Inflammation / Q000150:complications* / Q000276:immunology
keywords: atherosclerosis; blood pressure; infection; inflammasome; stenosis