Abstract: The present invention relates the field of reducing CD95-mediated cell motility in a subject, in particular for their use in the reduction of CD-95 mediated cancer cell motility, the reduction of CD95-mediated lymphocyte motility and/or B cell maturation, or the treatment of B-cell tumors, in a subject. The inventors identified a novel family of compounds having the ability to disrupt CD95/PLC?1 interaction and to neutralize the CD95-mediated calcium signaling pathway and cell migration in human peripheral blood lymphocytes (PBLs) and Th17 cells.

Abstract: The present invention relates the field of reducing CD95-mediated cell motility in a subject, in particular for their use in the reduction of CD-95 mediated cancer cell motility, the reduction of CD95-mediated lymphocyte motility and/or B cell maturation, or the treatment of B-cell tumors, in a subject. The inventors identified a novel family of compounds having the ability to disrupt CD95/PLC?1 interaction and to neutralize the CD95-mediated calcium signaling pathway and cell migration in human peripheral blood lymphocytes (PBLs) and Th17 cells.

Abstract: The present invention concerns the use of an inhibitor of interleukin-(IL-1), in particular of IL-1? and/or IL-1?, for the prevention or treatment of chronic histiocytic intervillositis (CHI) or a symptom associated thereof, eventually in combination with the use of at least one molecule conventionally prescribed to treat CHI and/or an interleukin-18 (IL-18) inhibitor. Said inhibitor of interleukin-1 (IL-1), in particular of IL-1? and/or IL-1?, may also be used for diagnosing in vitro CHI in a subject suspected of suffering from CHI or for monitoring in vitro the effectiveness of a treatment for CHI in a subject in need thereof.

Abstract: The present invention concerns clusterin for use in the treatment of thrombotic microangiopathies, and a pharmaceutical composition comprising clusterin for use in the treatment of thrombotic microangiopathies, said composition not comprising von Willebrand factor protease. The present invention also concerns an ex vivo method for stratifying a patient suffering, or likely to be suffering, from TMA, comprising the following steps: 1) measuring, in a biological sample from said patient, the amount LC of clusterin, and 2) comparing the amount Lc measured in step 1) with an amount Lref of clusterin by calculating the score S1=LC/Lref, in which: •If S1?1, the patient is considered to be likely to benefit from a treatment of the TMA with clusterin, •If S1>1, the patient is not considered to be likely to benefit from treatment of TMA with clusterin.

Abstract: Described herein are methods and compositions for treating autoimmunity and inflammatory conditions without non-specific suppression of the host immune system. In particular, the anti-OX40L antibodies described herein are unique in that they not only inhibit the differentiation of inflammatory T cells but also promote the generation and function of regulatory T cells by inducing IL-10 and inhibiting TNF-? and by reducing aberrant Th2 cell responses. Furthermore, the methods and compositions described herein eliminate or reduce aberrant T follicular helper cell—(Tfh) responses that may contribute to the pathogenicity of autoimmune disease.

Abstract: The present invention relates to a method for reducing CD95-mediated cell motility. To identify chemicals disrupting CD95/PLC?1 interaction, the inventors screened a chemical library of EMA/FDA-approved molecules against a protein-fragment complementation assay (PCA) monitoring the binding of CD95 to PLC?1. From this screen, five chemical molecules showed the ability to disrupt CD95/PLC?1 interaction and to neutralize the CD95-mediated calcium signaling pathway and cell migration in human peripheral blood lymphocytes (PBLs) and Th17 cells. Thus, the present invention relates to a method for reducing CD95-mediated cell motility, comprising administering the subject with at least one compound selected from the group consisting of HIV-protease inhibitors (e.g. ritonavir), diflunisal, anethole, rosiglitazone and daunorubicin.

Abstract: Described herein are methods and compositions for treating autoimmunity and inflammatory conditions without non-specific suppression of the host immune system. In particular, the anti-OX40L antibodies described herein are unique in that they not only inhibit the differentiation of inflammatory T cells but also promote the generation and function of regulatory T cells by inducing IL-10 and inhibiting TNF-? and by reducing aberrant Th2 cell responses. Furthermore, the methods and compositions described herein eliminate or reduce aberrant T follicular helper cell—(Tfh) responses that may contribute to the pathogenicity of autoimmune disease.

Abstract: Some embodiments are directed to a substance that inhibits P2Y12 receptor for use in the preventive treatment of systemic sclerosis in patients with Raynaud's phenomenon and a dysimmunity.

Abstract: Described herein are methods and compositions for treating autoimmunity and inflammatory conditions without non-specific suppression of the host immune system. In particular, the anti-OX40L antibodies described herein are unique in that they not only inhibit the differentiation of inflammatory T cells but also promote the generation and function of regulatory T cells by inducing IL-10 and inhibiting TNF-? and by reducing aberrant Th2 cell responses. Furthermore, the methods and compositions described herein eliminate or reduce aberrant T follicular helper cell—(Tfh) responses that may contribute to the pathogenicity of autoimmune disease.

Abstract: The present invention relates to methods and pharmaceutical compositions for the treatment of Th17-mediated diseases. In particular, the present invention relates to a method of treating a Th17-mediated disease in a subject in need thereof comprising administering to the subject a therapeutically effective amount of a CD95 antagonist.

Abstract: Described herein are methods and compositions for treating autoimmunity and inflammatory conditions without non-specific suppression of the host immune system. In particular, the anti-OX40L antibodies described herein are unique in that they not only inhibit the differentiation of inflammatory T cells but also promote the generation and function of regulatory T cells by inducing IL-10 and inhibiting TNF-? and by reducing aberrant Th2 cell responses. Furthermore, the methods and compositions described herein eliminate or reduce aberrant T follicular helper cell- (Tfh) responses that may contribute to the pathogenicity of autoimmune disease.

Abstract: Novel antigen-presenting cells, including but not limited to dendritic cells, that are loaded with antigens from dead or dying cells including allogenic cell lines, and the methods for making such antigen-presenting cells are described. These loaded antigen-presenting cells induce therapeutic immune responses in humans. Such loaded antigen-presenting cells are useful in the management of cancer. Antigen-loaded dendritic cells prepared as described here can prime naïve T cells to differentiate into effector cells able to recognize multiple and/or shared tumor antigens that are expressed either on the tumor cells that are used to load the dendritic cells and/or on other tumor cells. The cytotoxic T cells generated by exposure to antigen-loaded dendritic cells prepared as described here can be used in adoptive therapy. This induction of responses against multiple antigens shared between different cells, for instance tumor cells, as described here is important as it leads to broad immune responses.

Abstract: Novel antigen-presenting cells, including but not limited to dendritic cells, that are loaded with antigens from dead or dying cells including allogenic cell lines, and the methods for making such antigen-presenting cells are described. These loaded antigen-presenting cells induce therapeutic immune responses in humans. Such loaded antigen-presenting cells are useful in the management of cancer. Antigen-loaded dendritic cells prepared as described here can prime naïve T cells to differentiate into effector cells able to recognize multiple and/or shared tumor antigens that are expressed either on the tumor cells that are used to load the dendritic cells and/or on other tumor cells. The cytotoxic T cells generated by exposure to antigen-loaded dendritic cells prepared as described here can be used in adoptive therapy. This induction of responses against multiple antigens shared between different cells, for instance tumor cells, as described here is important as it leads to broad immune responses.

Abstract: The invention provides a method for treating an autoimmune disease in a subject by administering an interferon antagonist and a Flt3 ligand (Flt3L) antagonist. The invention also provides compositions containing one or more interferon antagonists, and one or more Flt3L antagonists, an in vitro assay for determining a subject's risk for developing an autoimmune disease, and kits for use, inter alia, with the assay.

Abstract: The invention provides a method for treating an autoimmune disease in a subject by administering an interferon antagonist and a Flt3 ligand (Flt3L) antagonist. The invention also provides compositions containing one or more interferon antagonists, and one or more Flt3L antagonists, an in vitro assay for determining a subject's risk for developing an autoimmune disease, and kits for use, inter alia, with the assay.

Abstract: The invention provides a method for treating an autoimmune disease in a subject by administering an interferon antagonist and a Flt3 ligand (Flt3L) antagonist. The invention also provides compositions containing one or more interferon antagonists, and one or more Flt3L antagonists, an in vitro assay for determining a subject's risk for developing an autoimmune disease, and kits for use, inter alia, with the assay.

Abstract: The invention provides a method for treating an autoimmune disease in a subject by administerineng an interfron antagonist and Flt3 ligand (Flt3L) antagonist. The invention also provides compositions containing one or more interferon antagonists, and one or more Flt3L antagonists, an in vitro assay for determining a subject's risk for developing an autoimmune disease, and kits for use, inter alia, with the assay.