The invention relates to a pharmaceutical combination and related methods for reducing tumor volume and/or increasing the survival of a cancer patient. The combination comprises an intravenous administration of a recombinant MVA encoding CD40L and an administration of an antagonist or agonist of an immune checkpoint molecule.

The present invention provides methods for isolating and cryopreserving tumor infiltrating lymphocytes (TILs) and producing therapeutic populations of TILs, including methods via use of a kit and a semi-automatic device for aseptic disaggregation, enrichment, and cryopreservation of a resected tumor prior to expansion of the TIL population. The present invention also provides methods for expansion, and/or stabilization of TILs, for instance UTILs, compositions involving the same and methods of treatment involving the same.

Embodiments of the present disclosure relate to a polynucleotide encoding a CAR comprising a cytoplasmic domain of CD4, or a CAR comprising SEQ ID NO: 17 in its intracellular domain, and the cytoplasmic domain of CD4 is located between a transmembrane domain of the CAR and a signaling or stimulatory domain, for example, CD3 zeta domain.

The present disclosure relates to identifying novel tumor immune evasion targets. A CRISPR activation screen was employed to identify novel checkpoint inhibitor targets, where upon upregulation, conferred tumor resistance to cytotoxic T cells in model cancer cell lines. Using MAGeCK and FDR analyses to identify candidate genes that were enriched in cancer cells, B3GNT2, MCL1, BCL2A1 and JUNB were identified as the most enriched after a pathway analysis of the top 576 genes prioritized by MAGeCK. Currently, these four genes have not been identified or suggested as possible checkpoint inhibitor targets. Provided herein are methods of targeting the expression or activity of B3GNT2, MCL1, BCL2A1 and JUNB using small molecule agents and/or gene editing methods with the aim of enhancing anti-tumor immunity in subjects in need thereof.

Provided herein are methods and compositions for the treatment of melanoma using anti-tumor immune cells treated with a PTD-MYC fusion protein (e.g., an HIV TAT-MYC fusion protein).

The disclosure discloses a kind of new NKT-like cell subpopulation, a therapeutical composition comprising the NKT-like cell subpopulation, and the medical use thereof. The disclosure also provides a preparation method of the NKT-like cell subpopulation. The disclosed NKT-like cell subpopulation has a strong antitumor effect, and can be adoptive transferred into a subject to treat the tumor in the subject after in vitro cultured and amplified.

The present invention refers to a method for obtaining a cell culture supernatant or a fraction thereof having a specific tumor antigen peptide repertoire having the steps of: a) exposing in suitable conditions a tumor cell culture expressing the specific tumor antigen peptide repertoire to a Pattern Recognition Receptor (PRR) agonist and/or to one inflammatory cytokine to increase the opening of connexin-hemichannels (CxH); b) collecting the cell culture supernatant; and c) optionally obtaining a fraction of the supernatant, wherein the supernatant has MHC class I and MHC class II peptides and non-classical MHC molecules (HLA-E).

A method is provided for treating a subject suffering from an infectious or neoplastic disease with immunotherapy. The method comprises determining the critical concentration of immune cells required to treat or eradicate an infectious or neoplastic disease in the subject using an in vitro assay of the present invention; and administering to the subject the critical concentration of immune cells determined in the assay.

This invention relates to the field of therapeutics. Most specifically invention provides methods of generating in vitro engineered immune cells conditionally expressing interleukin-12 (IL-12) and one or more immunomodulators under the control of a gene expression modulation system in the presence of activating ligand and uses for therapeutic purposes in animals.

The present invention relates to autologous dual-specific lymphocytes, methods of making and uses for the treatment of tumors. In particular, the invention relates to methods producing autologous dual-specific lymphocytes comprising an endogenous receptor for at least one tumor associated antigen and an exogenous receptor for a strong antigen.