Immediately after acute kidney injury (AKI), the immune system mounts a response that increases inflammation, causing additional kidney damage.
In a study published in the Journal of Clinical Investigation, researchers led by Li Li at the University of Virginia examined the role of the anti-inflammatory molecule adenosine in mediating this immune response.
Using a mouse model of AKI, they found that drugs that activate the adenosine 2A receptor (A2AR) protected kidneys and that mice with A2AR-deficient immune cells were more susceptible to kidney injury. Administration of immune cells that had been pre-treated with A2AR-activating drugs was also protective and could serve as a cell-based therapeutic in kidney injury.
In an accompanying commentary, Hamid Rabb of the Johns Hopkins University School of Medicine discusses how these findings could impact the development of immune-based therapies for AKI.
TITLE:Dendritic cells tolerized with adenosine A2AR agonist attenuate acute kidney injury
ACCOMPANYING COMMENTARY: The promise of immune cell therapy for acute kidney injury