Antagonist of IL-33 for use in methods of preventing ischemia-reperfusion injury of organs

摘要

Inflammation is a prominent feature of ischemia-reperfusion injury (IRI) characterized by leukocyte infiltration and tubular injury. However, the signals that initiate these events remain poorly understood. We have identified the nuclear allamine interleukin (IL) -33 as an initiator of tissue damage and as a major amplification factor of the innate immune response caused by experimental renal ischemia-reperfusion in mice. There is. In mice lacking IL-33, IRI is reduced, as evidenced by early reduction in tubular cytotoxicity and subsequent reduction in IFN-γ / IL-17A-producing neutrophil infiltration and maintenance of renal function. .. These findings indicate that endogenous IL-33 contributes to renal IRI by promoting iNKT cell recruitment and cytokine production, resulting in neutrophil infiltration and activation at the site of injury. Come to propose. Therefore, the present invention relates to IL-33 antagonists for use in methods of preventing ischemia-reperfusion injury in organs.