Patent classifications
A61K2239/55
THERAPY AND METHODS FOR INTRODUCING IMMATURE AND DENDRITIC CELLS AND/OR CYTOTOXIC T LYMPHOCYTE AND ANTI-TNF ANTIBODY FOR TREATMENT OF TUMORS
The invention relates to therapy and methods of applying the therapy to a patient. The invention includes the introduction of immature dendritic cells into the patient and the introduction of anti-TNF antibody into the patient. The immature dendritic cells are introduced intratumorally and/or through vessel and the anti-TNF antibody is introduced intratumorally and/or through vessel and/or subcutaneously. The immature dendritic cells can be formed by collecting monocyte cells from the patient and culturing the cells in a culture medium. The invention can be effective to regress, reduce or eliminate tumor cells in tumor tissue of the patients, including metastasized tumors. Further, the treatment of the invention is effective in the absence of conventional therapy, such as radiotherapy and chemotherapy.
METHOD FOR PREPARING NATURAL KILLER CELLS USING IRRADIATED PBMCS, AND ANTI-CANCER CELL THERAPEUTIC AGENT COMPRISING THE NK CELLS
Provided is a method for preparing natural killer cell with high efficiency using irradiated peripheral blood mononuclear cells, more particularly to a method for proliferating highly activated NK cells using a combination of irradiated peripheral blood mononuclear cells (PBMCs) and a CD16 antibody and an anti-cancer cell therapeutic composition containing the natural killer cells (NK cells) prepared thereby. Further provided is a method for large-scale proliferation of activated NK cells with high efficiency using a combination of irradiated peripheral blood mononuclear cells (PBMCs) and a CD16 antibody without the use of cancer cells or genetically modified feeder cells having safety issues as feeder cells. The highly purified and highly cytotoxic NK cells proliferated in large quantities can be used as an active ingredient of a cancer immunotherapeutic composition.
Inhibition of diacylglycerol kinase to augment adoptive T cell transfer
The present invention provides compositions and methods for inhibiting one or more diacylglycerol kinase (DGK) isoform in a cell in order to enhance the cytolytic activity of the cell. In one embodiment, the cells may be used in adoptive T cell transfer. For example, in some embodiments, the cell is modified to express a chimeric antigen receptor (CAR). Inhibition of DGK in T cells used in adoptive T cell transfer increases cytolytic activity of the T cells and thus may be used in the treatment of a variety of conditions, including cancer, infection, and immune disorders.
METHODS AND COMPOSITIONS TO AUGMENT EFFICACY AND REDUCE TOXICITY OF NON-ENGRAFTING, CD8-DEPLETED ALLOGENIC DONOR LYMPHOCYTE INFUSIONS
Provided herein are methods and compositions to augment the efficacy and reduce toxicity of non-engrafting, CD8-depeleted allogeneic donor lymphocyte infusions. The compositions comprise isolated leukocytes obtained from a donor subject that (i) are mismatched to a recipient subject for at least one human leukocyte antigen (HLA) Class II allele mismatch in the donor versus recipient (graft-versus-host) direction relative to the recipient subject or (ii) is mismatched to a recipient subject for at least one human leukocyte antigen (HLA) Class II allele mismatch in the donor versus recipient (graft-versus-host) direction relative to the recipient subject, is matched to the recipient for at least one human leukocyte antigen (HLA) Class II allele, and has CD4+ T cell immunity against an antigen present in a recipient subject.
Anti-PTK7 immune cell cancer therapy
Provided herein, in some embodiments, are methods and compositions (e.g., cell compositions) for the treatment of cancer, such as PTK7.sup.+ malignancies.
ROR1 targeting chimeric antigen receptor
The present disclosure relates to polynucleotides encoding a chimeric polypeptide comprising a c-Jun polypeptide, a ROR1-binding protein, and a truncated EGF receptor. Also provided are cells (e.g., T cells) expressing CARs comprising a ROR1-binding protein and overexpressing a c-Jun polypeptide. Overexpression of c-Jun in CAR T cells confers improved properties, e.g., reducing or preventing exhaustion.
CHIMERIC ANTIGEN RECEPTOR POLYPEPTIDES IN COMBINATION WITH TRANS METABOLISM MOLECULES MODULATING KREBS CYCLE AND THERAPEUTIC USES THEREOF
Disclosed herein are genetically engineered hematopoietic cells, which express one or more Krebs cycle modulating polypeptides, and optionally a chimeric receptor polypeptide (e.g., an antibody-coupled T cell receptor (ACTR) polypeptide or a chimeric antigen receptor (CAR) polypeptide) capable of binding to a target antigen of interest. Also disclosed herein are uses of the engineered hematopoietic cells for inhibiting cells expressing a target antigen in a subject in need thereof.
INTRACELLULAR DELIVERY OF BIOMOLECULES TO MODIFY IMMUNE RESPONSE
The present application provides T cells comprising an antigen and an adjuvant, methods of manufacturing such T cells, and methods of using such T cells, such as for modulating an immune response in an individual.
Immune cell compositions and methods of use
Disclosed herein are cells that are immune cells or precursor cells thereof, which cells recombinantly express a chimeric antigen receptor (CAR), and a dominant negative form of an inhibitor of a cell-mediated immune response of the immune cell, wherein the CAR binds to a cancer antigen. Also disclosed herein are T cells that recognize and are sensitized to a cancer antigen, which T cells recombinantly express a dominant negative form of an inhibitor of a T cell-mediated immune response. Additionally provided are methods of using such cells to treat cancer in a subject in need thereof.
TREATMENT OF NSCLC PATIENTS WITH TUMOR INFILTRATING LYMPHOCYTE THERAPIES
The present invention provides improved and/or shortened processes and methods for preparing TILs in order to prepare therapeutic populations of TILs with increased therapeutic efficacy for the treatment of non-small cell lung carcinoma (NSCLC), wherein the NSCLC is refractory to treatment with an anti-PD-1 antibody and/or anti-PD-L1 antibody and/or VEGF inhibitor, or wherein the NSCLC has a predetermined tumor proportion score (TPS).