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.
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Visan, I. ILCs in liver pathology. Nat Immunol 14, 1023 (2013). https://doi.org/10.1038/ni.2717
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DOI: https://doi.org/10.1038/ni.2717