A liver receptor helps restore immune cells for repair in mice

In an experiment in mice undergoing surgical removal of 70% of the liver, researchers tracked how the organ healed. In normal mice, liver regeneration prompted strong activation and infiltration of T cells and Kupffer cells, which are specialised liver immune cells. In contrast, mice lacking the farnesoid X receptor (FXR), a regulatory protein, showed weakened immune activation and reduced immune cell entry during regrowth, despite having higher baseline numbers. Regenerating livers normally replenish Kupffer cells by drawing in circulating monocytes, a type of white blood cell, and by triggering resident Kupffer cells to divide. Lacking FXR impaired both processes, which the authors report likely delayed liver regeneration. The researchers also observed that impaired monocyte recruitment in aged mice may contribute to a decline in regenerative capacity with age.