IL13 and renal fibrosis: Although the exact cellular mediators and downstream mechanisms of this deleterious IL-33 effect in renal fibrosis were not explored in these studies (41, 42), pro-fibrotic effects of chronically activated ILC2s via production of IL-13 were described in the liver and lung (43, 44), indicating that systemic ILC2-directed therapies might comprise a substantial risk for side effects which are likely to be determined by dose, duration, and context of cytokine application.