The present invention relates to engineered extra-cellular vesicle internalizing receptors that have the ability to enhance uptake, processing, and presentation to T-cells of tumor-associated antigens by an antigen-presenting cell. It further relates to vectors or antigen presenting cells expressing said receptors, composition and uses thereof for the prevention and/or treatment of a cancer.

Genetically modified mice and methods and compositions for making and using the same are provided, wherein the genetic modification comprises humanization of an FcγRI protein.

The present invention discloses chimeric antigen receptors that specifically recognize and bind to SLe A carbohydrate antigen with high specificity and selectivity. The invention further provides lymphocytic cells, such as T cells, comprising said CARs, compositions comprising said cells or CARs as well as uses thereof.

Provided herein are recombinant nucleic acids encoding T cell receptor (TCR) fusion proteins (TFPs), modified human immune cells expressing the encoded molecules, and methods of use thereof for the treatment of diseases, including cancer.

The present invention relates to a chimeric antigen receptor comprising a c-Met binding domain, and a use thereof. The chimeric antigen receptor comprising a c-Met domain, of the present invention, can be effectively usable as an agent for treating various diseases associated with c-Met expression.

Disclosed are compositions and methods for treating disease or condition caused or exacerbated by S100A9 activity, such as myelodysplastic syndromes (MDS) using a composition comprising an effective amount of a CD33/S100A9 inhibitor.

This disclosure relates to a chimeric antigen receptor for binding with a target antigen. The chimeric antigen receptor comprises at least one antigen specific targeting region including a multispecific antibody evolved from a wild-type antibody or a fragment thereof and having at least one of: (a) a decrease in activity in the assay at the normal physiological condition compared to the wild-type antibody or the fragment thereof, and (b) an increase in activity in the assay under the aberrant condition compared to the wild-type antibody or the fragment thereof. A method for using the chimeric antigen receptor and cytotoxic cells for cancer treatment is also provided. A method for producing the chimeric antigen receptor is also provided.

The present invention is directed to heterodimeric anti-LAG-3×anti-CTLA-4. Also provided are nucleic acid compositions that encode the antibodies, expression vector compositions that include the nucleic acids, and host cells that include the expression vector compositions.

The present invention provides a human CD16.sup.+ natural killer cell line and a CAR-expressing human CD16.sup.+ natural killer cell line. These human CD16.sup.+ natural killer cell line and a CAR-expressing human CD16.sup.+ natural killer cell line does not include synthetic, genetically modified or purposely deliberately delivered polynucleotide encoding the CD16 receptor and are non-tumorigenic cell lines. Therefore, this human CD16.sup.+ natural killer cell line and a CAR-expressing human CD16.sup.+ natural killer cell line might provide considerable long-term safety for disease treatment.

Provided herein are genetically modified (GM) natural killer (NK) cells and methods of producing populations of GM NK cells. Further provided herein are methods of using the GM NK cells described herein, to, e.g., suppress the proliferation of tumor cells, or to inhibit pathogen infection, e.g., viral infection. In certain alternatives, GM NK cells provided herein lack expression of CBLB, NKG2A and/or TGFBR2 and/or function or show reduced expression and/or function of CBLB, NKG2A and/or TGFBR2. In certain alternatives, GM NK cells provided herein comprise modified CD16.