The patent badge is an abbreviated version of the USPTO patent document. The patent badge does contain a link to the full patent document.
The patent badge is an abbreviated version of the USPTO patent document. The patent badge covers the following: Patent number, Date patent was issued, Date patent was filed, Title of the patent, Applicant, Inventor, Assignee, Attorney firm, Primary examiner, Assistant examiner, CPCs, and Abstract. The patent badge does contain a link to the full patent document (in Adobe Acrobat format, aka pdf). To download or print any patent click here.
Patent No.:
Date of Patent:
Nov. 19, 2024
Filed:
Jan. 24, 2019
Inserm (Institut National DE LA Santé ET DE LA Recherche Médicale), Paris, FR;
Université DE Poitiers, Poitiers, FR;
Centre Hospitalier Universitaire DE Poitiers, Poitiers, FR;
Centre National DE LA Recherche Scientifique (Cnrs), Paris, FR;
André Herbelin, Poitiers, FR;
Jean-Marc Gombert, Poitiers, FR;
Maroua Ferhat, Salt Lake City, UT (US);
Antoine Thierry, Poitiers, FR;
Jean-Philippe Girard, Toulouse, FR;
INSTITUT NATIONAL DE LA SANTE ET DE LA RECHERCHE MEDICALE (INSERM), Paris, FR;
CENTRE HOSPITALIER UNIVERSITAIRE DE POITIERS, Poiters, FR;
UNIVERSITE DE POITIERS, Poiters, FR;
CENTRE NATIONAL DE LA RECHERCHE SCIENTIFIQUE, Paris, FR;
Abstract
Inflammation is a prominent feature of ischemia-reperfusion injury (IRI) characterized by leukocyte infiltration and renal tubular injury. However, the signals that initiate these events remain poorly understood. The inventors identify the nuclear alarmin interleukin (IL)-33 as an initiation factor of tissue injury and also as a major amplification factor of the innate immune response triggered by experimental kidney ischemia-reperfusion in mice. In mice lacking IL-33, IRI is reduced, as attested by early decreased tubular cell injury, and by subsequent decreased infiltration of IFN-γ/IL-17A-producing neutrophils and preservation of renal functions. These findings led the inventors to propose that endogenous IFN-33 contributes to kidney IRI by promoting iNKT cell recruitment and cytokine production, resulting in neutrophil infiltration and activation at the injury site. Accordingly, the present invention relates to antagonists of IL-33 for use in methods for preventing ischemia reperfusion injury in an organ.