Type 2 innate lymphoid cells are protective against hepatic ischemia reperfusion injury

Background & AimsAlthough type 2 innate lymphoid cells (ILC2s) were originally found to be liver-resident lymphocytes, the role and importance of ILC2 in liver injury remains poorly understood. In current study, we sought determine whether is an important regulator hepatic ischemia/reperfusion (IRI).MethodsILC2 deficient mice (ICOS-T or NSG) genetically modified ILC2s used investigate murine IRI. Interactions between eosinophils macrophages studied co-culture. The human was assessed immunocompromised mouse model IRI.ResultsAdministration IL-33 prevented IRI association with reduction neutrophil infiltration inflammatory mediators liver. IL-33-treated had elevated numbers ILC2s, regulatory T (Tregs). Eosinophils, but not Tregs required for IL-33-mediated hepatoprotection mice. Depletion substantially abolished protective effect IRI, indicating play critical roles protection. Adoptive transfer ex vivo-expanded improved function attenuated histologic damage subjected Mechanistic studies combining genetic adoptive approaches identified a through promoting IL-13-dependent induction anti-inflammatory IL-5-dependent elevation Furthermore, vivo expansion by ameliorated IRI.ConclusionThis study provides insight into mechanisms ILC2-mediated protection that could serve as therapeutic targets treat acute injury.Impact implicationsWe report are regulators (IRI). Through manipulation macrophage eosinophil phenotypes, mitigate inflammation during We propose have potential tool protecting against lay foundation translation therapy disease.