Abstract: T-cell lymphomas are a heterogeneous group of malignancies involving T lymphocytes and generally characterized by a poor prognosis. Among them, cutaneous T-cell lymphomas involve primarily the skin. Mycosis fungoides and Sezary syndrome are the most frequent cutaneous T-cell lymphomas. The inventors studied the regulatory T phenotype of Sezary cells and showed the expression of CCR8 (CD198) by Sezary cells and other T-cell lymphoma cell lines. CCR8 therefore appears as a useful diagnostic, prognostic and follow-up marker, and as a potential therapeutic target in T-cell lymphomas. Therapeutic depletion of CCR8-expressing cancer cells would eliminate tumor cells and also activate the anti-tumor immunity in T-cell lymphomas.

Abstract: Novel anti-human CD25 antibodies or antigen-binding fragments thereof and their use for treating cancer and infectious diseases. Also, a nucleic acid encoding an anti-human CD25 antibody or antigen-binding fragment thereof, and a fusion protein including an isolated anti-human CD25 antibody or antigen-binding fragment thereof. Further, a pharmaceutical composition including an isolated anti-human CD25 antibody or antigen-binding fragment thereof.

Abstract: Novel anti-human CD25 antibodies and their use for treating cancer and infectious diseases. Also, a nucleic acid encoding an anti-human CD25 antibody or an antigen-binding fragment thereof, and a fusion protein including an isolated anti-human CD25 antibody or an antigen-binding fragment thereof. Further, a pharmaceutical composition including an isolated anti-human CD25 antibody or an antigen-binding fragment thereof.

Abstract: The invention relates to antibodies against human CD39 and use thereof for inhibiting T regulatory cells (Treg) activity. More particularly CD39 antibodies may be used for the treatment or prevention of cancers and infectious diseases.

Abstract: The present invention concerns the combination of CTLA4 and IL-17B inhibitors, especially for the treatment of patients and diseases resistant to anti-CTLA4 therapies.

Abstract: The invention relates to novel IL-17B antagonist antibodies and their use in the diagnosis or treatment of IL-17B mediated diseases.

Abstract: CD38 is also expressed in a variety of malignant hematological diseases, including multiple myeloma. In the present invention, the inventors have generated a new antibody against CD38 that could be suitable for producing bispecific antibodies as well as CAR-T cells. In particular, the inventors report the development of Bi38-3, a new bispecific T cell engager that targeted CD38 on MM cells and recruited cytotoxic T cells through the CD3?. Bi38-3 lacked the Fc region of natural mAb, which contributes to resistance processes, but triggered T cells to proliferate, release cytokine and lyse CD38 positive MM cells in vitro. Similarly, Bi38-3 induced autologous T cells to eliminate tumor plasma cells isolated from MM patients both at diagnosis and at relapse. The cytotoxicity triggered by Bi38-3 was restricted to cells expressing high levels of CD38 and preserved the integrity of T, B and NK lymphocytes in vitro. Importantly, Bi38-3 rapidly reduced tumor cells in an MM1.S xenograft mouse model of human MM.

Abstract: Novel anti-CD25 antibodies and antigen-bind fragments thereof that do not inhibit the binding of interleukin-2 (IL-2) to CD25, and the use thereof for treating cancer or an infectious disease. Also, fusion proteins including the antibodies and antigen-bind fragments, nucleic acids encoding the antibodies and antigen-bind fragments, and an expression vectors including the nucleic acids. Further, pharmaceutical compositions including the fusion proteins or the antibodies and antigen-bind fragments.

Abstract: The present invention relates to a method for ex vivo generating and expanding MHCII restricted CD4+ Foxp3+ regulatory T cells, and therapeutic uses thereof. The inventors here demonstrated the optimal conditions for inducing Foxp3 expression in naive CD3+ CD4+ TCR??+ MHCII restricted T following polyclonal or following antigen-specific activation. They also developed an experimental procedure to generate autologous CD8+ T cell lines functionally committed to lyse tumor-antigen specific FOXP3 expressing TCR??+ MHCII restricted T cells, pathogenic CD4+ T cells that favour tumor cell immune evasion. In particular, the present invention relates to a method for generating ex vivo MHCII restricted CD4+ Foxp3+ regulatory T cells having the following phenotype: CD3+ CD4+ Foxp3+.

Abstract: The present invention relates to a method for ex vivo generating and expanding ?? Foxp3+ regulatory T cells, and therapeutic uses thereof. The inventors performed the induction of Foxp3+ expression in ex vivo human induced tumor-antigen specific CD4? TCR?? unrestricted T cells and the induction of autologous CD8-mediated T-cell responses against tumor-antigen specific FOXP3 expressing CD4+ TCR?? unrestricted T cells. The inventors developed a method to ex vivo generated and expanded antigen specific Foxp3 expressing CD3+ TCR??+ unrestricted T cells, committed to exclusively exert regulatory activity, whichever culture condition of stimulation is. In particular, the present invention relates to a method for generating ex vivo ?? Foxp3+ regulatory T cells having the following phenotype: CD3+ TCR??+ Foxp3+.

Abstract: Sézary syndrome is a rare, aggressive, and leukemic form of cutaneous T-cell lymphoma (CTCL) characterized by erythroderma associated with generalized peripheral lymphadenopathy and circulating clonal malignant T cells called Sézary cells. Current animal models of Sézary syndrome are not satisfactory since no cutaneous symptoms or occurrence of metastases could be observed. Now the inventors developed a new non-human animal model that repeat the major cutaneous symptoms of the human disease. This model could be suitable for screening new drugs and biomarkers of the disease.

Abstract: Among regulatory T cells, natural regulatory T cells (nTregs) ensure the control of self-tolerance and are currently tested in clinical trials in autoimmune diseases and allogeneic hematopoietic stem cell transplantation. Here the inventors show that based on CD39/CD26 markers, the human nTreg population is comprised of 5 major cell subsets each representing a distinct state of maturation. Phenotypic and genetic characteristics of the subsets illustrate the structural parental maturation between subsets which further correlates with expression of regulatory factors. Importantly, the inventors also show that blood nTreg CD39/CD26 profile, remaining constant over a 2year period in healthy persons but varying between individuals, represents a novel biomarker for monitoring chronic diseases, as illustrated in their preliminary study on AI (dermatomyositis, rheumatoid arthritis and leukemias).

Abstract: The present invention relates to a method for ex vivo generating and expanding ?? Foxp3+ regulatory T cells, and therapeutic uses thereof. The inventors performed the induction of Foxp3+ expression in ex vivo human induced tumor-antigen specific CD4+ TCR?? unrestricted T cells and the induction of autologous CD8-mediated T-cell responses against tumor-antigen specific FOXP3 expressing CD4+ TCR?? unrestricted T cells. The inventors developed a method to ex vivo generated and expanded antigen specific Foxp3 expressing CD3+ TCR??+ unrestricted T cells, committed to exclusively exert regulatory activity, whichever culture condition of stimulation is. In particular, the present invention relates to a method for generating ex vivo ?? Foxp3+ regulatory T cells having the following phenotype: CD3+ TCR??+ Foxp3+.

Abstract: The present invention relates to monoclonal antibodies that bind to the CD160-TM isoform. The inventors developed new monoclonal antibodies which bind to the CD160-TM isoform but dot not bind to the CD160 GPI-anchored isoform not to the CD160 soluble isoform. In particular, the antibodies of the present invention are suitable for amplifying NK cell activation and therefore cytotoxic functions NK cells.

Abstract: The present invention relates to a CD39 antagonist for use for inhibiting the immunosuppressive effects of a CD39-expressing cancerous cell.

Abstract: The invention relates to antibodies against human CD39 and use thereof for inhibiting T regulatory cells (Treg) activity. More particularly CD39 antibodies may be used for the treatment or prevention of cancers and infectious diseases.

Abstract: The invention relates to antibodies against human CD39 and use thereof for inhibiting T regulatory cells (Treg) activity. More particularly CD39 antibodies may be used for the treatment or prevention of cancers and infectious diseases.

Abstract: The present invention relates to monoclonal antibodies that bind to the CD160-TM isoform. The inventors developed new monoclonal antibodies which bind to the CD160-TM isoform but dot not bind to the CD160 GPI-anchored isoform not to the CD160 soluble isoform. In particular, the antibodies of the present invention are suitable for amplifying NK cell activation and therefore cytotoxic functions NK cells.

Abstract: The invention relates generally to antagonists of IL-17 isoforms and their uses in diagnosis and therapy, especially for the treatment or prevention of cancers or autoimmune and chronic inflammatory diseases.

Abstract: The present invention relates to therapeutic uses of ex vivo generated Foxp3+ regulatory T cells. The inventors showed the presence of Foxp3+ expressing T cells in tumor infiltrating lymphocytes (TILs) isolated from luminal-B breast cancer. The inventors performed an ex vivo generation and expansion of specific CD3+ TCRy8+ expressing Foxp3: CD3+ TCRy8+ T cells maintain their Foxp3 level and their suppressive activity, after a further 21-day-culture. They also showed that tumor Ag-specific CD3+ TCR Va24+ T cells maintain their ability to perform suppressive function in pro-inflammatory conditions. In particular, the present invention relates to immunotherapeutic uses of at least one of ex vivo generated Foxp3+regulatory T cells population selected among a MHCII restricted CD4+Foxp3+regulatory T cells population, a y8 Foxp3+regulatory T cells population and an invariant Foxp3+regulatory T cells population.