The present disclosure provides therapeutic agents comprising oncolytic vaccinia viruses and NK cells, and uses thereof for preparation of drugs for treatment of tumors and/or cancers. The active ingredients of the therapeutic agents comprise an oncolytic vaccinia virus and NK cells, wherein the oncolytic vaccinia virus can selectively replicate in tumor cells.

Disclosed herein are methods for treating cancer comprising administering CAR-modified immune cells and at least one Retinoic Acid Receptor agonist.

A method for producing natural killer cells is disclosed. The method comprises isolating peripheral blood mononuclear cells (PBMCs) from a blood sample; isolating at least one of CD56+ cells and/or CD3/CD56+ cells from the PBMCs; and co-culturing the at least one of CD56+ cells and/or CD3/CD56+ cells with a combination of feeder cells in the presence of a cytokine. A composition for treating cancer is also disclosed. The composition comprises the CD56+ natural killer cells produced by the disclosed method and a cytokine.

Episomally transfected primary mesenchymal stem cells (MSC) express a polypeptide consisting of an antigenic polypeptide (e.g., one or more polypeptides) relating to a pathogen (e.g., one or more virus, bacterium, or parasite). The antigenic polypeptide can have the amino acid sequence of a natural polypeptide from the pathogen or an amino acid sequence differing from the natural sequence by one or more conservative amino acid substitutions. Uses and method for treating or preventing infections with episomally transfected primary MSC also are described.

Disclosed herein are methods for treating cancer comprising administering CAR-modified immune cells and at least one Retinoic Acid Receptor and/or Retinoid X Receptor active agent.

The present invention relates to chimeric immune receptor molecules for reducing or eliminating tumors. The chimeric receptors are composed a C-type lectin-like natural killer cell receptor, or a protein associated therewith, fused to an immune signaling receptor containing an immunoreceptor tyrosine-based activation motif. Methods for using the chimeric receptors are further provided.

Methods and compositions are provided for combined transplantation of a solid organ and hematopoietic cells to a recipient, where tolerance to the graft is established through development of a persistent mixed chimerism. An individual with persistent mixed chimerism, usually for a period of at least six months, is able to withdraw from the use of immunosuppressive drugs after a period of time sufficient to establish tolerance.

The present invention relates to TCR molecules which recognise neopeptides produced as a result of the cancer-associated ?1A frameshift mutation in human TGF?RII. The TCR molecules are capable of binding a peptide of SEQ ID NO: 1 when said peptide is presented by a Class I MHC, and comprise an ?-chain domain and a ?-chain domain, each chain domain comprising three CDR sequences, wherein a) CDRs 1, 2 and 3 of the ?-chain domain have the sequences of SEQ ID NOs: 2, 3 and 4 respectively; and b) CDRs 1, 2 and 3 of the ?-chain domain have the sequences of SEQ ID NOs: 5, 6 and 7 respectively, and wherein one or more of said CDR sequences may optionally be modified by substitution, addition or deletion of 1 or 2 amino acids. Nucleic acid molecules encoding such TCRs are provided, as are soluble TCR molecules with these CDR sequences. The nucleic acid molecules of the invention can be used to modify immune effector cells to express a TCR as defined herein, and such modified immune effector cells are useful in therapy for cancer, as are soluble TCRs as defined above.

The invention provides methods of preventing or treating ocular diseases and conditions by adoptive transfer of plasmacytoid dendritic cells and related compositions.

The invention provides chimeric antigen receptors (CARs) that specifically bind to the T-cell immunoglobulin and mucin domain 1 (TIM-1) protein. The invention further relates to modified immune cells, e.g., T or NK cells, comprising such CARs, CAR-encoding nucleic acids, CAR-encoding vectors, and methods of making such compositions. The invention further relates to methods for therapeutic use of these CARs and modified immune cells for the treatment of a condition, disorder, or disease associated with cells expressing TIM-1 (e.g., cancer).