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-?/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.

Abstract: The inventors aim to assess IL-33 and HMGB1 contributions as alarmins to I/R injury following solid organ transplantation in particular liver transplantation. This study was conducted from a prospective biological collection and a clinical database of 40 liver transplant recipients in Tours hospital center. Serum IL-33 and HMGB1 levels were determined at graft reperfusion, at the end of the liver transplantation and at postoperative day 1 and 3. A post-reperfusion liver biopsy was systematic. Serum IL-33 increase is associated with: i) severe-moderate liver lesions; ii) an early allograft dysfunction; iii) a post-reperfusion syndrome occurrence; iv) a post liver transplantation acute kidney injury occurrence. Serum HMGB1 increase is associated with: i) an early allograft dysfunction; ii) a post-reperfusion syndrome occurrence. IL-33 and HMGB1 thus contribute as alarmins to I/R injury in human liver transplantation. Their serum levels are predictive of I/R injury severity and its clinical impact.

Abstract: The present invention relates to a method for discontinuing a treatment with a TKI by determining the number and/or frequency of innate CD8(+) T-cells in subject and concluding that the treatment with a TKI should be discontinued when the number and/or frequency of innate CD8 T-cells is higher than the predetermined reference value. Inventors evaluated whether innate CD8(+) T-cells are an early target of CML therapy success. Among peripheral blood effector CD8(+) T-cells, inventors shown that both number nd/or frequency and functional signatures of innate CD8(+) T-cells are enhanced as early as 3 months of therapy. Strikingly, they observe that patients with high innate CD8(+) T-cell number and/or frequency at 3 months and/or diagnosis achieve a DMR earlier than patients with low innate CD8(+) T-cell number. Furthermore, a higher number and/or frequency of high innate CD8(+) T-cell patients achieved a stable DMR for over 2 years.

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-?/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.

Abstract: The use of interleukin 7 or T cells pre-incubated in the presence of IL-7 for preparing a drug or pharmaceutical composition for treating an auto-immune disease, particularly an auto-immune disease induced by a defect in CD4+ T cell immunoregulation, is disclosed.

Abstract: The use of interleukin 7 or T cells pre-incubated in the presence of IL-7 for preparing a drug or pharmaceutical composition for treating an auto-immune disease, particularly an auto-immune disease induced by a defect in CD4+ T cell immunoregulation, is disclosed.