Hypertension: It is Autoimmunity that Underlies its Development in Humans
Reporter: Aviva Lev-Ari, PhD, RN
Autoimmunity Underlies the Development of Hypertension (page 792)
It is now widely recognized that both human and experimental hypertension are linked to activation of the innate and adaptive immune system. Experimental models have allowed investigators to determine the relative importance of immune cell subsets, inflammatory cytokines, and proinflammatory signaling pathways to regulate blood pressure through renal, central, and vascular mechanisms. In humans, small clinical studies suggest that targeting the immune system can benefit hypertensive patients, particularly those with concurrent chronic inflammatory diseases.
Through these studies, a concept has emerged that the underpinnings of hypertension may be autoimmune in nature. This is partly supported by growing evidence that autoantigens are initiators of experimental hypertension, and that circulating autoantibodies are associated with human essential hypertension. In this issue of Hypertension, Mathis et al used an experimental mouse model of autoimmune disease (systemic lupus erythematosus) to address the question of whether autoimmunity per se underlies the development of hypertension. The results show that administration of a mouse anti-CD20 antibody (the equivalent of rituximab, used to deplete B lymphocytes in humans with chronic inflammatory disease) at an age preceding the development of systemic lupus erythematosus prevents the development of the hypertension and renal disease associated with this model. These data extend our understanding of the role for adaptive immunity in hypertension and further support the concept that autoimmunity can be an important factor in the pathogenesis of hypertension
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