Memories that last in hypertension

Abstract

In recent years, it has become clear that the immune system contributes to the genesis of hypertension. Hypertensive stimuli, such as angiotensin II, DOCA-salt, and norepinephrine, cause T cells and monocytes/macrophages to accumulate in the kidney and vasculature. These cells release inflammatory cytokines, such as IL-6, interferon-γ, and IL-17, that promote renal and vascular dysfunction. These cytokines also promote angiotensinogen production in the proximal tubule and Na(+) retention in the distal nephron and contribute to renal fibrosis and glomerular damage. For several years, we have observed accumulation of memory T cells in the kidney and vasculature. Given the propensity for memory cells to produce cytokines such as interferon-γ and IL-17, interventions to prevent the formation or renal accumulation of specific memory T cell subsets could prevent end-organ damage and blood pressure elevation in response to hypertensive stimuli.

Keywords: CD70; T cells; adaptive immunity; cytokines; immunological memory.

Fig. 1.

The dynamics of T cell immune responses. The classical adaptive T cell immune response is characterized by an initial expansion of naïve T cells upon antigen (Ag) presentation. The majority of activated effector T cells ultimately undergo apoptosis with a subset of antigen-specific memory T cells remaining. These memory cells are characterized by the presence of a T cell receptor that is capable of recognizing the original antigen and can respond rapidly and efficiently to a second antigenic stimulus.