Abstract: The invention relates to methods for the prediction and the treatment of risk of acute graft versus host disease. The inventors demonstrated that an alteration of CD73-mediated regulatory function of DP8? Tregs could contribute to the acute GvHD pathophysiology. In particular, the present invention relates to method of determining whether a subject has or is at 0 a risk of developing graft-versus-host disease (GvHD) comprising the steps of: i) determining the level of CD73 expression by DP8? TREGS in a sample obtained from the subject, ii) comparing the level determined at step i) with a predetermined reference value wherein detecting differential between the level of CD73 expression by DP8? TREGS determined at step i) and the predetermined reference value is indicative of whether a subject has or is at a risk of developing graft-versus-host disease (GvHD).

Abstract: The invention relates to a method comprising a step of determining the number, concentration and/or proportion of T lymphocytes with a CD4+ CD8??low phenotype and further expressing CCR6 and/or CXCR6, for (i) diagnosing, (ii) prognosing outcome of, or (iii) predicting the risk of developing a disease related to a decrease of F. prau. The invention also concerns the treatment of said disease by administering a population of these specific T lymphocytes. The Inventors have indeed identified two markers, CCR6 and CXCR6, enabling to select a population of F. prau-specific cells among CD4+ CD8??low T lymphocytes, from a blood sample and without needing to assess their F. prauspecificity. T lymphocytes with a CD4+ CD8??low CCR6+ CXCR6+ phenotype are for example significantly decreased in IBD patients. The disease related to a decrease of F. prauis particularly an inflammatory bowel disease (IBD), such as Crohn's disease.

Abstract: The present invention relates to enhancing, modulating or stimulating the immune response to MMP-2 expressing tumors, including melanoma, and to the modulation and application of immune modulators and MMP-2 peptides for melanoma or other MMP-2 expressing tumor vaccines. The invention provides methods and means to activate an effective response to MMP-2 expressing tumors and modulate the ability of MMP-2 to skew CD4+ T cell responses toward that of TH2 cells, which are less effective mediators of tumor cell clearance than TH1 cells. Methods and assays are provided for screening for compounds, agents, or peptides capable of enhancing or activating immune responses, particularly to melanoma.

Abstract: The present invention relates to enhancing, modulating or stimulating the immune response to MMP-2 expressing tumors, including melanoma, and to the modulation and application of immune modulators and MMP-2 peptides for melanoma or other MMP-2 expressing tumor vaccines. The invention provides methods and means to activate an effective response to MMP-2 expressing tumors and modulate the ability of MMP-2 to skew CD4+ T cell responses toward that of TH2 cells, which are less effective mediators of tumor cell clearance than TH1 cells. Methods and assays are provided for screening for compounds, agents, or peptides capable of enhancing or activating immune responses, particularly to melanoma.

Abstract: The present invention relates to enhancing, modulating or stimulating the immune response to MMP-2 expressing tumors, including melanoma, and to the modulation and application of immune modulators and MMP-2 peptides for melanoma or other MMP-2 expressing tumor vaccines. The invention provides methods and means to activate an effective response to MMP-2 expressing tumors and modulate the ability of MMP-2 to skew CD4+ T cell responses toward that of TH2 cells, which are less effective mediators of tumor cell clearance than TH1 cells. Methods and assays are provided for screening for compounds, agents, or peptides capable of enhancing or activating immune responses, particularly to melanoma.

Abstract: The present invention relates to enhancing, modulating or stimulating the immune response to MMP-2 expressing tumors, including melanoma, and to the modulation and application of immune modulators and MMP-2 peptides for melanoma or other MMP-2 expressing tumor vaccines. The invention provides methods and means to activate an effective response to MMP-2 expressing tumors and modulate the ability of MMP-2 to skew CD4+ T cell responses toward that of TH2 cells, which are less effective mediators of tumor cell clearance than TH1 cells. Methods and assays are provided for screening for compounds, agents, or peptides capable of enhancing or activating immune responses, particularly to melanoma.

Abstract: Peptides derived from MMP-2 metalloproteinase that form T cell epitopes when presented by MHC Class I molecules. Anti-tumor therapy using these peptides.

Abstract: The present invention relates to a purified soluble HLA-E molecule, characterized in that: it is a monomeric protein, it presents a sequence identity of at least 80% with membrane-bound HLA-E (SEQ ID NO: 1), it has a molecular weight from about 36 kDa to about 42 kDa, it binds to the CD94/NKG2A receptor.

Abstract: The invention relates to peptides forming epitopes T of the antigen MMP-2, presented by MHC class I. Said peptides can especially be used in antitumoral immunotherapy.

Abstract: The invention concerns the use of immunogenic peptides representing T epitopes presented by the MHC I, derived from Melan-A, MAGE-A6, gp 100, tyrosinase and NY-ESO-1 antigens for the diagnosis or treatment of melanomas in HLA-B35 subjects.

Abstract: New tumor rejection antigen precursors, and the nucleic acid molecules which code for them, are disclosed. These tumor rejection antigen precursors are referred to as NAG tumor rejection antigen precursors, and the nucleic acid molecules which code for them are referred to as NAG coding molecules. Various diagnostic and therapeutic uses of the coding sequences and the tumor rejection antigen precursor molecules are described.

Abstract: New tumor rejection antigen precursors, and the nucleic acid molecules which code for them, are disclosed. These tumor rejection antigen precursors are referred to as NAG tumor rejection antigen precursors, and the nucleic acid molecules which code for them are referred to as NAG coding molecules. Various diagnostic and therapeutic uses of the coding sequences and the tumor rejection antigen precursor molecules are described.

Abstract: New tumor rejection antigen precursors, and the nucleic acid molecules which code for them, are disclosed. These tumor rejection antigen precursors are referred to as NAG tumor rejection antigen precursors, and the nucleic acid molecules which code for them are referred to as NAG coding molecules. Various diagnostic and therapeutic uses of the coding sequences and the tumor rejection antigen precursor molecules are described.