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: 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 present invention discloses novel active polypeptide fragments of human IL-33 corresponding to natural forms generated by the proteases of human neutrophils (cathepsin G, elastase 2, proteinase 3), as well as the use thereof as a drug, in particular for the treatment of infectious diseases, inflammatory diseases, atherosclerosis, cardiovascular diseases, obesity, or cancer.

Abstract: The present invention concerns a method of inducing IL-2-free proliferation of ?? T cells using a combination of a ?? T cell activator and IL-33 for use in therapy of infection, cancer, autoimmunity as well as other diseases.

Abstract: The present invention discloses novel active polypeptide fragments of human IL-33 corresponding to natural forms generated by the proteases of human neutrophils (cathepsin G, elastase 2, proteinase 3), as well as the use thereof as a drug, in particular for the treatment of infectious diseases, inflammatory diseases, atherosclerosis, cardiovascular diseases, obesity, or cancer.

Abstract: Described herein are chemokine-binding domains of THAP-family polypeptides and pharmaceutical compositions which include a polypeptide comprising a chemokine-binding domain of a THAP-family polypeptide. Also disclosed are methods of binding chemokines, inhibiting the activity of chemokines, detecting chemokines, and reducing the symptoms associated with a chemokine mediated or influenced condition by contacting the chemokine with an agent that includes a polypeptide comprising a chemokine binding domain of a THAP-family polypeptide.

Abstract: Described herein are chemokine-binding domains of THAP-family polypeptides and pharmaceutical compositions which include a polypeptide comprising a chemokine-binding domain of a THAP-family polypeptide. Also disclosed are methods of binding chemokines, inhibiting the activity of chemokines, detecting chemokines, and reducing the symptoms associated with a chemokine mediated or influenced condition by contacting the chemokine with an agent that includes a polypeptide comprising a chemokine binding domain of a THAP-family polypeptide.

Abstract: Described herein are chemokine-binding domains of THAP-family polypeptides and pharmaceutical compositions which include a polypeptide comprising a chemokine-binding domain of a THAP-family polypeptide. Also disclosed are methods of binding chemokines, inhibiting the activity of chemokines, detecting chemokines, and reducing the symptoms associated with a chemokine mediated or influenced condition by contacting the chemokine with an agent that includes a polypeptide comprising a chemokine binding domain of a THAP-family polypeptide.

Abstract: The invention relates to genes and proteins of the THAP (THanatos (death)-Associated Protein) family comprising a THAP domain, and their use in diagnostics, treatment of disease, and in the identification of molecules for the treatment of disease. The invention also relates to the Par4 protein and SLC chemokine pathways, including the interaction of Par4 and SLC with THAP family proteins, and the recruitment and localization of Par4 to PML nuclear bodies.

Abstract: The invention relates to genes and proteins of the THAP (THanatos (death)-Associated Protein) family comprising a THAP domain, and their use in diagnostics, treatment of disease, and in the identification of molecules for the treatment of disease. The invention also relates to the Par4 protein and SLC chemokine pathways, including the interaction of Par4 and SLC with THAP family proteins, and the recruitment and localization of Par4 to PML nuclear bodies.

Abstract: Aspects of the present invention relate to NF-HEV nuclear factor genes and polypeptides. Other aspects related to the use of NF-HEV nuclear factor genes and polypeptides. Other aspects related to the use of NF-HEV nuclear factor polynucleotides and polypeptides expressed in endothelial cells from chronically inflamed tissues, particularly in high endothelial venules endothelial cells (HEVECs) and endothelial cells from HEV-like vessels and small blood vessels, in connection with rheumatoid arthritis and Crohn's disease. Aspects of the invention also relates to drug screening assays for identifying compounds capable of modulating NF-HEV activity, wherein such compounds can be used in inhibiting or preventing chronic inflammation.

Abstract: Among the methods and compositions described herein are methods of ameliorating one or more symptoms associated with a chemokine-mediated or influenced condition by providing to a subject an agent that includes a polypeptide comprising a chemokine binding domain of a THAP-family polypeptide.

Abstract: Described herein are chemokine-binding domains of THAP-family polypeptides and pharmaceutical compositions which include a polypeptide comprising a chemokine-binding domain of a THAP-family polypeptide. Also disclosed are methods of binding chemokines, inhibiting the activity of chemokines, detecting chemokines, and reducing the symptoms associated with a chemokine mediated or influenced condition by contacting the chemokine with an agent that includes a polypeptide comprising a chemokine binding domain of a THAP-family polypeptide.

Abstract: Described herein are chemokine-binding domains of THAP-family polypeptides and pharmaceutical compositions which include a polypeptide comprising a chemokine-binding domain of a THAP-family polypeptide. Also disclosed are methods of binding chemokines, inhibiting the activity of chemokines, detecting chemokines, and reducing the symptoms associated with a chemokine mediated or influenced condition by contacting the chemokine with an agent that includes a polypeptide comprising a chemokine binding domain of a THAP-family polypeptide.

Abstract: Described herein are chemokine-binding domains of THAP-family polypeptides and pharmaceutical compositions which include a polypeptide comprising a chemokine-binding domain of a THAP-family polypeptide. Also disclosed are methods of binding chemokines, inhibiting the activity of chemokines, detecting chemokines, and reducing the symptoms associated with a chemokine mediated or influenced condition by contacting the chemokine with an agent that includes a polypeptide comprising a chemokine binding domain of a THAP-family polypeptide.

Abstract: The invention relates to genes and proteins of the THAP family comprising a THAP domain, and their use in diagnostics, treatment of disease, and in the identification of molecules for the treatment of disease. The invention also relates to uses of THAP-type chemokine-binding agents, such as THAP-family proteins, as a nuclear receptors for a chemokines and to methods for the modulation (stimulation or inhibition) of transcription, cell proliferation and cell differentiation as well as methods for identifying for compounds which modulate THAP-chemokine interactions.

Abstract: The invention relates to genes and proteins of the THAP (THanatos (death)-Associated Protein) family comprising a THAP domain, and their use in diagnostics, treatment of disease, and in the identification of molecules for the treatment of disease. The invention also relates to the Par4 protein and SLC chemokine pathways, including the interaction of Par4 and SLC with THAP family proteins, and the recruitment and localization of Par4 to PML nuclear bodies.

Abstract: The invention concerns a method for making food products with open-cell internal texture by baking in an oven a paste conventionally kneaded such as, dough for bread, pizza or the like. The invention is characterized in that it consists at least in preparing said dough without kneading to obtain a viscous paste with low consistency; pressurising it followed by sudden depressurisation through a nozzle adapted to generate a foam which can then be baked in the oven. The invention also concerns a device for implementing said method comprising hoppers (1) and vats (2), a mixer (3), a swelling machine (4) which pressurises the paste before depressurising it through a nozzle (5) and a tunnel oven (8). The invention is useful for making gluten-free bread.

Abstract: The present invention is directed to the SUT-2 and SUT-3 sulfate/anion exchanger polypeptides expressed in high endothelial venules endothelial cells (HEVECs). The invention also relates to drug screening assays for identifying compounds capable of inhibiting sulfate/anion transport and L-selectin mediated lymphocyte adhesion to high endothelial venules. Such compounds may be useful in the treatment of inflammatory conditions.

Abstract: A telephone amplifier and attenuator circuit comprising an amplifier and an attenuator inserted in the transmit channel and an attenuator inserted in the receive channel of a telephone set. The speech signals conveyed by the transmit and receive channels are detected and added together for forming a sum control signal. The transmit amplifier is controlled by the detected transmit signal and the two attenuators are controlled in opposite directions by the sum control signal. In the preferred embodiment, the amplifier and attenuators are formed respectively by a balanced modulator and by balanced modulators inserted in the loop of negative feed back amplifiers.