Abstract 406: Direct Angiotensin AT2-Receptor Stimulation Modifies T-Cell Differentiation

Angiotensin II is known to activate T-cells via the AT1-receptor. T-cells also possess AT2-receptors (AT2Rs). However, the functional role of AT2Rs in T-cells has not been investigated. This study tested the hypothesis that AT2R stimulation modulates T helper (Th) cell differentiation. For this purpose, naive T-cells were isolated from spleen and lymph nodes of C57BL/6 mice, sorted, polarized in vitro under Th0, Th1, Th17 and regulatory T-cell (Treg) conditions and simultaneously treated with the AT2R agonist C21 (1μM) or vehicle for 4 days. 24 hours after the last treatment, expression of cytokines characteristic for pro-inflammatory Th1 cells (IFNγ) and Th17 cells (IL-17), or anti-inflammatory Treg (FoxP3) were determined on mRNA (qRT-PCR) and protein (FACS analysis) level. AT2R stimulation during polarization of naive T-cells decreased mRNA levels of IFNγ (in TH1 polarized T-cells: 2.2±0.4x105 [vehicle] versus 0.1±0.001x105 [C21] fold increase; p Similar results were obtained for protein expression of IFNγ (6.5±0.5x105 [vehicle] versus 4.0±0.7x105 [C21] cells; p From our data we conclude that AT2R stimulation modifies T-cell differentiation resulting in a composition of T-cell subsets with less pronounced pro-inflammatory properties.