Key result
Transferring renal antigen-presenting cells from hypertensive mice increases blood pressure and reduces natriuresis via T cells.
Why the study?
Does the transfer of renal antigen-presenting cells from Ang II-hypertensive mice increase blood pressure and promote sodium retention in recipient mice?
Does the transfer of renal antigen-presenting cells from Ang II-hypertensive mice increase blood pressure and promote sodium retention in recipient mice?
Renal antigen-presenting cells from Ang II-hypertensive mice can transfer hypertension and promote sodium retention in a T cell-dependent manner.
May implicate renal antigen-presenting cells in hypertension via T cells; leaves open translation to human disease.
Ablation of APCs prevented Ang II-induced hypertension, NKCC2 activation, and preserved natriuresis. Transfer of renal APCs from Ang II-mice increased BP and reduced natriuresis in recipient mice; renal APCs from normotensive mice or splenic APCs from Ang II-infused mice had no effect. The effect of renal APCs was dependent on the presence of T cells. Renal APCs from Ang II-mice showed preferential destination to the kidney and increased expression of cytokines.
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Araos et al. (2025) studied Ang II-induced hypertension. Transfer of renal APCs from Ang II-mice vs. Renal APCs from normotensive mice or splenic APCs from Ang II-infused mice was evaluated on Blood pressure and natriuresis. Transfer of renal antigen-presenting cells from Ang II-hypertensive mice increased blood pressure and reduced natriuresis in recipient mice, an effect dependent on the presence of T cells.
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