Provided is an anti-B7-H4 antibody containing a VH, wherein the VH contains the following CDRs or a mutation thereof: CDR1 as shown in the amino acid sequence of SEQ ID NO: 4 or 5, CDR2 as shown in the amino acid sequence of SEQ ID NO: 15, and CDR3 as shown in the amino acid sequence of SEQ ID NO: 24 or 25, and wherein the mutation is an insertion, deletion or substitution of 3, 2 or 1 amino acid(s) in the amino acid sequences of the CDRs. The antibody has the activity of binding to human B7-H4 and cynomolgus monkey B7-H4. The antibody still retains the activity of binding to human B7-H4 and cynomolgus monkey B7-H4 when prepared into a B7-H4CD3 bispecific antibody, and has a strong killing effect on tumor cells. The antibody induces a very low expression of nonspecific cytokines such as IL-6 and IFN-, and exhibits a strong in vivo anti-tumor activity.

The present invention relates to a bispecific molecule targeting NK cells, and relates to a method for resisting transplant immune rejection caused by NK cells, and particularly relates to a method for providing antibodies targeting NK cells or for providing cells which secrete the antibodies targeting NK cells, so as to resist transplant immune rejection caused by NK cells of an individual receiving a transplant. The present invention also relates to a CRISPR/Cas-related methods, compositions, and components for editing a target nucleic acid sequence or modulating the expression of a target nucleic acid sequence.

The present disclosure provides improved compositions for adoptive T cell therapies targeting CD33 for treating, preventing, or ameliorating at least one symptom of a cancer, infectious disease, autoimmune disease, inflammatory disease, and immunodeficiency, or condition associated therewith. The present disclosure also relates to adoptive T cell therapies targeting CD33 and another target antigen for treating, preventing, or ameliorating at least one symptom of a cancer, infectious disease, autoimmune disease, inflammatory disease, and immunodeficiency, or condition associated therewith.

An isolated human NKT cell or a plurality of cells thereof, having reduced or no detectable expression of endogenous beta-2-microglobulin (B2M); endogenous MHC class II-associated invariant chain (Ii); or both. Methods to generate the cell or cells, and methods of treatment using the cell or cells are also provided.

The present disclosure relates to T cells capable of co-expressing T cell receptors (TCR) together with CD8 polypeptides and the use thereof in adoptive cellular therapy. The present disclosure further provides for modified CD8 sequences, vectors, and associated methods thereof.

Provided herein is a nucleic acid molecule comprising 5 to 3 a first nucleotide sequence encoding a safety switch polypeptide comprising a suicide moiety; a second nucleotide sequence encoding FOXP3; and a third nucleotide sequence encoding a chimeric antigen receptor (CAR); particularly wherein said first, second, and third nucleotide sequences are separated by nucleotide sequences encoding self-cleavage sequences. Also provided are constructs, vectors and cells comprising the nucleic acid molecule, and methods and uses for expressing the encoded polypeptides in cells, particularly in immune cells useful in adoptive cell therapy (ACT).

The present disclosure provides methods for treating cancer comprising administering 13-isobutyl-4-methyl-10-(pyrimidin-2-ylamino)-1,2,4,7,8,13-hexahydro-6H-indazolo[5,4-a]pyrrolo[3,4-c]carbazol-6-one or N-[(E)-(3-methylphenyl)methylideneamino]-6-morpholin-4-yl-2-(2-pyridin-2-ylethoxy)pyrimidin-4-amine to a subject in combination with adoptive cell therapy (ACT) or a personalized cancer vaccine to a subject.

Various embodiments of the present disclosure provide therapeutic compositions and associated methods for improved hematopoietic stem cell transplantations, including methods to enhance protection from graft versus host disease while maintaining effective immune responses such as graft versus tumor immune responses.

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.

D domain (DD) containing polypeptides (DDpp) that specifically bind targets of interest (e.g., BCMA, CD123, CS1, HER2, AFP, and AFP p26) are provided, as are nucleic acids encoding the DDpp, vectors containing the nucleic acids and host cells containing the nucleic acids and vectors. DDpp such as DDpp fusion proteins, are also provided as are methods of making and using the DDpp. Such uses include, but are not limited to diagnostic and therapeutic applications.