Methods and compositions for treating cancers (e.g., neural cancers) by dendritic cell vaccination are provided herein.

The present invention relates to augmenting the effects of adoptive T cell therapy, such as TVAX Immunotherapy, using adjunct treatment with an oncolytic virus, such as a vaccinia virus, to treat various types of cancer or other proliferative disorders. Immunomodulatory compounds can be used to further augment to effects of the therapy.

The present invention provides a cell-based platform for controllable, regionalized, and cost-effective delivery of immunomodulator and other therapeutic proteins, which is widely applicable in cancer immunotherapy.

A chimeric antigen receptor targeting to NKG2DL, its encoding sequence, and its modified immune response cells, and the preparation and application of them. This invention constructs a chimeric antigen receptor targeting to NKG2DL and its modified immune response cell based on the NKG2D molecule, and the novel modified immune response cells can effectively target a variety of tumor cells, especially the expression of NKG2DL positive tumor cells, and can be used to prepare preparations for the treatment of tumors. The preparation of the modified immune response cells of the target NKG2DL is easy, and the immune response cells modified by the target NKG2DL have high killing rate to the tumor cells.

The present invention regards methods and/or compositions related to Natural Killer T cells that are engineered to harbor an expression construct that encodes IL-2, IL-4, IL-7, and/or IL-15 and additionally or alternatively comprise a chimeric antigen receptor (CAR). In specific embodiments, the CAR is a CAR that targets the GD2 antigen, for example in neuroblastoma

Disclosed herein are polynucleotides encoding ligand-inducible gene switch polypeptides, and systems comprising gene switch polypeptides for modulating the expression of a heterologous gene and an interleukin in a host cell. The compositions, methods and systems described herein facilitate ligand dependent expression of polypeptides including but not limited to cytokines and antigen binding polypeptides.

Provided are combination therapies for treating and preventing relapse of a tumor and infectious diseases in a subject, as well as methods for use thereof. The combination therapies comprise an Hsp70 based pharmaceutical ingredient and at least one further immunotherapeutic agent that specifically inhibits and/or preferably binds to an immune checkpoint molecule or tumor immune microenvironment immune regulator. Furthermore, a kit and methods of using the combination therapies of the invention are described.

The present invention provides in certain embodiments compositions comprising at least one CD200 inhibitor, and methods of reversing or modulating immune suppression in a patient having a disease or disorder arising from abnormal cell growth, function or behavior, which method comprises administering to a patient in need thereof a CD200 inhibitor composition.

Disclosed herein are polynucleotides encoding ligand-inducible gene switch polypeptides, and systems comprising gene switch polypeptides for modulating the expression of a heterologous gene and an interleukin in a host cell. The compositions, methods and systems described herein facilitate ligand dependent expression of polypeptides including but not limited to cytokines and antigen binding polypeptides.

Provided herein are methods of treating an IDH mutant cancer in a subject comprising administering to the subject a therapeutically effective amount of a composition comprising an all-trans retinoic acid (ATRA). In some embodiments, the methods increase an NK-cell-mediated immune response and/or a T cell-mediated immune response to the cancer. In some embodiments, the cancer is a glioma or a chondrosarcoma. In some embodiments, the expression of one or more NKG2D ligands (e.g., ULBP1 and ULBP3) is increased in a tumor microenvironment of the cancer. In some embodiments, CCL2 production, the number of NK cells, and/or apoptosis of tumor cells is increased in a tumor microenvironment of the cancer. In some embodiments, the subject has an IDH1 mutation at arginine 132 or an IDH2 mutation at arginine 172. In some embodiments, method reduces growth of a tumor.