Regulation of T-cell function by endogenously produced angiotensin II.
Ontology highlight
ABSTRACT: The adaptive immune response and, in particular, T cells have been shown to be important in the genesis of hypertension. In the present study, we sought to determine how the interplay between ANG II, NADPH oxidase, and reactive oxygen species modulates T cell activation and ultimately causes hypertension. We determined that T cells express angiotensinogen, the angiotensin I-converting enzyme, and renin and produce physiological levels of ANG II. AT1 receptors were primarily expressed intracellularly, and endogenously produced ANG II increased T-cell activation, expression of tissue homing markers, and production of the cytokine TNF-alpha. Inhibition of T-cell ACE reduced TNF-alpha production, indicating endogenously produced ANG II has a regulatory role in this process. Studies with specif
SUBMITTER: Hoch NE
PROVIDER: S-EPMC2643984 | biostudies-literature | 2009 Feb
REPOSITORIES: biostudies-literature
ACCESS DATA