The immune system in hypertension

Abstract

While hypertension has predominantly been attributed to perturbations of the vasculature, kidney, and central nervous system, research for almost 50 yr has shown that the immune system also contributes to this disease. Inflammatory cells accumulate in the kidneys and vasculature of humans and experimental animals with hypertension and likely contribute to end-organ damage. We and others have shown that mice lacking adaptive immune cells, including recombinase-activating gene-deficient mice and rats and mice with severe combined immunodeficiency have blunted hypertension to stimuli such as ANG II, high salt, and norepinephrine. Adoptive transfer of T cells restores the blood pressure response to these stimuli. Agonistic antibodies to the ANG II receptor, produced by B cells, contribute to hypertension in experimental models of preeclampsia. The central nervous system seems important in immune cell activation, because lesions in the anteroventral third ventricle block hypertension and T cell activation in response to ANG II. Likewise, genetic manipulation of reactive oxygen species in the subfornical organ modulates both hypertension and immune cell activation. Current evidence indicates that the production of cytokines, including tumor necrosis factor-α, interleukin-17, and interleukin-6, contribute to hypertension, likely via effects on both the kidney and vasculature. In addition, the innate immune system also appears to contribute to hypertension. We propose a working hypothesis linking the sympathetic nervous system, immune cells, production of cytokines, and, ultimately, vascular and renal dysfunction, leading to the augmentation of hypertension. Studies of immune cell activation will clearly be useful in understanding this common yet complex disease.

Therapeutic effects of Wharton jelly‐derived mesenchymal stem cells on rat abortion models

“…3,4 Imbalance of Th1 and Th2 cytokine production of peripheral lymphocytes were found in RPL women. Th1 cells secreted various cytokines, including IL-2 and IFN-γ, which mediated cellular immunity.…”

Renin, Genes, MicroRNAs, and Renal Mechanisms Involved in Hypertension

“…The immune system and inflammation are involved in the genesis and progression of hypertension, [121][122][123][124][125] with evidence linking the sympathetic nervous system, immune cells, production of cytokines, and, ultimately, vascular and renal dysfunction, so leading to the augmentation of hypertension. 124 NADPH oxidase, by generating superoxide and thence other reactive oxygen species, is critical for many forms of hypertension.…”

“…124 NADPH oxidase, by generating superoxide and thence other reactive oxygen species, is critical for many forms of hypertension. In hypertension, renal proteins that have been oxidatively modified by γ-ketoaldehydes (isoketals) stimulate dendritic cells to produce interleukin-6, -1β, and -23 as well as costimulatory proteins CD80 and CD86 that then cause T cell proliferation, interferon-γ, and interleukin-17A production and hypertension.…”

Souffrance au travail et enjeux de santé : le rôle charnière de l’inflammation et du stress oxydant

“…Cette mobilisation cellulaire répondrait à la formation de protéines modifiées, soit par les espèces réactives à l'oxygène (Harrison, 2014 ;Trott, 2014), soit du fait des perturbations du métabolisme du glucose et des lipides (résistance à l'insuline et formation de produits de glycation avancée) sous l'action des cytokines proinflammatoires (Vasdev, 2011). Enfin, les métallo-protéinases de la matrice contribuent au remaniement de la paroi artérielle et à sa rigidification (Park, 2012).…”

“…Les cellules inflammatoires s'accumulent dans les régions péri-vasculaires du rein et au niveau des glomérules (Harrison, 2012). Elles perturbent la fonction rénale et contribuent au développement de la maladie (Harrison 2012(Harrison , 2014Trott, 2014). Enfin, au niveau cérébral, l'activation de la NADPH oxydase et la production d'espèces réactives de l'oxygène seraient à l'origine d'un renforcement de l'activité sympathique (Harrison, 2014) et perturberaient le fonctionnement des organes responsables de la régulation centrale de la tension artérielle et de l'inflammation (Konior, 2014).…”