The present invention provides modified antigen-specific immune cells expressing an exogenous CD 160 protein. In some embodiments, the modified antigen-specific immune cell further comprises a functional exogenous receptor, such as an engineered TCR or a CAR. The present invention also provides methods of modulating CD 160 activity in antigen-specific immune cells. The present invention also provides methods and pharmaceutical compositions for cancer treatment using the modified antigen-specific immune cells and the modulators of CD 160 activity described herein.

The present disclosure is directed recombinant T cell receptors capable of binding an NY-ESO-1 epitope and nucleic acid molecules encoding the same. In some embodiments, the nucleic acid molecules further comprise a second nucleotide sequence, wherein the second nucleotide sequence or the polypeptide encoded by the second nucleotide sequence inhibits the expression of an endogenous TCR. Other aspects of the disclosure are directed to vectors comprising the nucleic acid molecule and cells comprising the recombinant TCR, the nucleic acid molecule, or the vector. Still other aspects of the disclosure are directed to methods of using the same. In some embodiments, the methods comprise treating a cancer in a subject in need thereof.

Provided are chimeric antigen receptors having the hinge, transmembrane region, and/or intracellular domain of LILRB1, or functional fragments or variants thereof. Also provided herein are cells comprising the LILRB1 based receptors, and methods of making and using same.

Abstract: Compositions and methods are provided relating to the design, screening and therapeutic use of designed binding proteins that specifically interact with an MHC/peptide complex. Proteins that specifically bind to an MHC/antigenic peptide complex of interest are designed through engineering of protein structure and screening assays. Selected binders are screened to minimize cross-reactivity with self-MHC-peptides. The antigen binding region thus developed can be formatted into a therapeutic agent that activates cytolytic pathways.

Disclosed are immunotherapeutic compositions and the concurrent use of combinations of such compositions for the improved induction of therapeutic immune responses and/or for the prevention, amelioration and/or treatment of disease, including, but not limited to, cancer and infectious disease.

The present application relates to an attenuated oncolytic virus strain, an oncolytic virus vaccine and a drug for treating tumors by combining the oncolytic virus vaccine with immune cells. The present application provides a new attenuated oncolytic virus strain by a site-directed mutation of a matrix protein M of a VSV wild-type virus. On the basis of the attenuated oncolytic virus strain, the present application further provides a vaccine that can be used in tumor treatment. On the basis of the vaccine, the present application further provide a drug that can effectively treat multiple kinds of tumors by combining the vaccine with immune cells.

Provided herein are methods for delaying or inhibiting T cell maturation or differentiation in vitro for a T cell therapy, comprising contacting one or more T cells from a subject in need of a T cell therapy with an AKT inhibitor and at least one of exogenous Interleukin-7 (IL-7) and exogenous Interleukin-15 (IL-15), wherein the resulting T cells exhibit delayed maturation or differentiation. In some embodiments, the method further comprises administering the one or more T cells to a subject in need of a T cell therapy.

The presently disclosed subject matter provides methods and compositions for enhancing immune responses toward tumor and pathogen antigens. It relates to fusion polypeptide that can be expressed in cells (e.g., immunoresponsive cells comprising an antigen-recognizing receptor) to improve the activity and/or efficiency of the cells. In certain embodiments, the fusion polypeptide comprises an extracellular domain and a transmembrane domain of a co-stimulatory ligand, and an intracellular domain of a co-stimulatory molecule.

The present invention relates to T cell receptors (TCR) against cancer/testis antigens NY-ESO-1 and CT83 presented by multiple HLA molecules. The preferred TCRs of the invention deriving from human T cells demonstrates high affinity and antigen specificity in vitro and in vivo. The present invention also relates to the modulation of TCR-T CAR-T cell signaling and functional persistence in cancer immunotherapy.

The present invention concerns compositions and methods related to approaches to render ineffective Th1 T cells resistant to the inhibitory cytokine milieu present in a cancer microenvironment. In particular embodiments, tumor-specific T cells are modified to employ a chimeric receptor that binds inhibitory/suppressive cytokines and converts their intracellular consequences to a Th1 immunostimulaotyr/activating signal. In specific embodiments, the T cells employ a chimeric antigen receptor having exodomains for IL10, IL13 and/or IL4 fused with the signal transducing endodomains for IL2 and/or IL7.