Hepatic fibrosis develops as a consequence of persistent inflammation in chronic liver infections or metabolic disease. In Immunity, Wirtz and colleagues show that interleukin 33 (IL-33) released from liver cells in the context of stress is a key mediator of hepatic fibrosis. Type 2 innate lymphoid cells (ILC2) are present in the liver of naive mice and are activated by IL-33 to produce IL-13, which in turn stimulates hepatic stellate cells to produce extracellular matrix proteins and leads to pathologic remodeling of the tissue. Other IL-33–reponsive, IL-13–producing cells, such as basophils and mast cells, were not essential for IL-33–mediated pathology, suggesting that the IL-33–ILC2 axis is the key mediator of hepatic fibrosis in several in vivo models of liver injury or infection.

Immunity 39, 357–371 (2013)