Provided are methods for generating γδ T cells from induced pluripotent stem cells. Also provided are genetically engineered iPSCs, γδ T cells, CAR-γδ T cells, and methods of using the same.

Provided are method for generating αβ T cells from induced pluripotent stem cells. Also provided are genetically engineered iPSCs, αβ T cells, CAR-αβ T cells, and methods of using the same.

Provided herein, in some embodiments, are methods and compositions (e.g., cell compositions) for the treatment of cancer.

There is provided an effector immune cell which expresses a cell surface receptor or receptor complex which specifically binds an antigen recognition receptor of a target immune cell; which effector immune cell is engineered such that when a synapse is formed between the effector immune cell and the target immune cell, the capacity of the effector immune cell to kill the target immune cell is greater than the capacity of the target immune cell to kill the effector immune cell. There is also provided the use of such a cell in methods for treating cancer, preventing allograft rejection and GVHD.

Provided in the present disclosure is a method for using a four-plasmid system to prepare modified immune effector cells. The method comprises: forming a lentivirus by using four plasmids within 293T cells, extracting and obtaining the lentivirus, then transfecting immune effector cells by using the lentivirus, and expressing a chimeric antigen receptor. Also provided in the present disclosure is a use of the immune effector cell obtained by using the described method and of a composition containing the immune effector cell.

The present invention provides therapeutics for the treatment of CD22-positive cancers such as B-cell acute lymphoblastic leukemia (B-ALL). In particular, the present invention provides an anti-CD22 monoclonal antibody whose scFv as a part of chimeric antigen receptors (CAR) T-cells can target the first Ig extracellular domain of the CD22 antigen, the farthest domain from the membrane, for use in the treatment of CD22-positive cancers.

A chimeric antigen receptor, comprising an amino acid sequence shown in SEQ ID NO. 1. A nucleic acid encoding the chimeric antigen receptor, a vector comprising the nucleic acid, an immune effector cell comprising the chimeric antigen receptor, the nucleic acid molecule and/or the vector, a method for preparing the immune effector cell, a composition comprising the immune effector cell, and use of the chimeric antigen receptor.

There are provided, inter alia, compositions and methods for treatment of cancer. The methods include administering to a subject in need a therapeutically effective amount of a Bruton's tyrosine kinase (BTK) antagonist and a ROR-1 antagonist. Further provided are pharmaceutical compositions including a BTK antagonist, ROR-1 antagonist and a pharmaceutically acceptable excipient. In embodiments, the BTK antagonist is ibrutinib and the ROR-1 antagonist is cirmtuzumab.

Disclosed are chimeric antigen receptors (CARs) comprising Centyrins (i.e. CARTyrins), transposons encoding CARs and CARTyrins of the disclosure, cells modified to express CARs and CARTyrins of the disclosure, as well as methods of making and methods of using same for adoptive cell therapy.

Engineered NK cells (NK-CAR cells) for targeted immunotherapy of certain cancers are disclosed. Chimeric antigen receptor polypeptides (CAR), and nucleic acids encoding the same, as well as methods of generation of the NK-CAR cells are provided herein. The NK-CAR cells as disclosed herein are capable of, inter alia, binding to TCR receptors, and are useful for treating lymphomas. Also provided are methods of treating cancers using NK-CAR cells.