Provided is a ??T cell for securing the purity and number of cells sufficient for treatment. Also provided is a method of generating the ??T cell. More specifically, provided are homogeneous ??T cells excellent in that the ??T cells are not affected by exhaustion of the cells. The foregoing is achieved by ??T cells obtained by subjecting induced pluripotent stem cells (iPS cells) to differentiation induction treatment. Specifically, the foregoing is achieved by ??T cells generated by subjecting iPS cells having a rearranged ??TCR gene (??TCR-type iPS cells) to differentiation induction treatment. According to the method of generating the ??T cell of the present invention, there can be provided ??T cells and a cell population of ??T cells that have an excellent function of having antigen-specific cytotoxic activity in a MHC-unrestricted manner, and that are more homogeneous and have a higher effect than ??T cells separated from peripheral blood.

Novel anti-effector moiety antibodies or antigen binding domains thereof and CARs that contain such effector moiety antigen binding domains, either with or without one or more booster elements, and host cells expressing the receptors, and nucleic acid molecules encoding the receptors are provided herein, as well as methods of use of same in a patient-specific immunotherapy that can be used to treat solid tumor cancers and other diseases and conditions.

The present disclosure relates to the field of cell therapy, and more specifically, to improving CAR and/or TCR function through cytokine signaling or cytokine receptor signaling.

The present invention relates to population of T cells with reduced expression of SIGLEC15, wherein the T cells are derived from sentinel lymph nodes in a subject having a cancer. The invention also relates to methods for obtaining such T cells, as well as to their use in therapy and pharmaceutical compositions comprising such T cells.

Chimeric antigen receptors (CAR) that bind Preferentially Expressed Antigen in Melanoma (PRAME) ALY(SEQ ID NO: 94)/HLA-A2 are disclosed. The CAR can be used to treat PRAME/HLA-A2 expressing cancers such as the t(8;21), Inv(16), and KMT2A-r forms of acute myeloid leukemia (AML).

Provided is a chimeric antigen receptor, comprising an antigen binding region, a transmembrane domain and an intracellular signaling region. The antigen binding region comprises an antibody specifically targeting CD7, and the intracellular signaling region consists of a co-stimulatory domain, a primary signal transduction domain, and a ?C chain or intracellular region thereof. Also provided are an engineered immune cell comprising the chimeric antigen receptor and a pharmaceutical composition thereof, and use of the engineered immune cell/pharmaceutical composition for treating cancers.

The present invention includes compositions and methods for treating AML utilizing bispecific CARs. In certain aspects, the invention includes a bispecific split CAR which binds CD13 and TIM-3 on AML cells. In one aspect, the invention provides a bispecific chimeric antigen receptor (CAR) comprising a first antigen binding domain capable of binding CD13, a first intracellular domain, a second antigen binding domain capable of binding TIM-3, a transmembrane domain, and a second intracellular domain.

The present invention provides compositions and methods for treating cancer in a human. The invention includes a chimeric receptor which comprises an CD64 binding domain, a transmembrane domain, and a CD3zeta signaling domain.

The present invention encompasses genetically-modified immune cells (and populations thereof) expressing a microRNA-adapted shRNA (shRNAmiR) that reduces the expression of a target endogenous protein. Methods for reducing the expression of an endogenous protein in an immune cell are also provided wherein the method comprises introducing a shRNAmiR that targets the endogenous protein. Using shRNAmiRs for knocking down the expression of a target protein allows for stable knockdown of expression of endogenous proteins in immune cells.

The present invention provides a bispecific CS1-BCMA CAR-T cell and an application thereof. Specifically, the present invention provides a bispecific CAR, which comprises CS1 scFv and BCMA scFv, and a 4-1BB co-stimulatory domain and a CD3 activation domain. The bispecific CAR-T cell in the present invention has a significant killing effect on CS1 positive target cells and BCMA positive target cells, and can secrete IFN- against target cells and significantly inhibit the growth of RPMI8226 xenograft tumor in an in vivo experiment. The present invention further provides a preparation method and an application of the bispecific CAR-T cell.