The present invention generally relates to antigen binding receptors capable of specific binding to an Fc domain comprising the amino acid mutation P329G according to EU numbering. The present invention also relates to T cells, transduced with a antigen binding receptor which is recruited by specifically binding to/interacting with the mutated Fc domain of therapeutic antibodies. Furthermore, the invention relates to a kit comprising the transduced T cells of the invention and/or nucleic acid molecules, vectors encoding the antigen binding receptors of the present invention and tumor targeting antibodies comprising a mutated Fc domain.

Genetically modified cells, including a recombinant nucleic acid expression construct including a first nucleic acid sequence region encoding a chimeric antigen receptor (CAR) that includes an extracellular antigen-binding domain recognizing a carcinoembryonic antigen (CEA) protein, a second nucleic acid sequence region encoding a checkpoint inhibitory molecule, and a third nucleic acid sequence region encoding an immune stimulatory cytokine. In some aspects, the genetically modified cells are T cells or NK cells, preferably cytotoxic T lymphocytes. Anti-CEA CAR-T cells or anti-CEA CAR-NK cells preferentially recognize a membrane-bound CEA protein and express a checkpoint inhibitory molecule and/or an immune stimulatory interleukin in proximity to tumor tissue. Medical use of the cells may relate to treatment of a medical disorder associated with the presence of pathogenic cells expressing CEA, preferably cancer cells, more preferably cancer cells of solid malignancies.

Disclosed are compositions and methods for treating autoimmune diseases such as lupus, including immune cells expressing at least a chimeric antigen receptor (CAR) polypeptides that binds CD83 and uses thereof for suppressing and/or killing autoreactive cells in a subject having an autoimmune disease.

Disclosed are isolated or purified T cell receptors (TCRs) having antigenic specificity for human p53.sup.R273C or human p53.sup.Y220C. Related polypeptides and proteins, as well as related nucleic acids, recombinant expression vectors, host cells, populations of cells, and pharmaceutical compositions are also provided. Also disclosed are methods of detecting the presence of cancer in a mammal and methods of treating or preventing cancer in a mammal.

The present invention provides a pharmaceutical composition comprising cells expressing a chimeric receptor, for use in combination with administration of an antigen-binding molecule, wherein the chimeric receptor comprises an extracellular domain, the extracellular domain comprises an extracellular domain of an immunoreceptor, an extracellular domain variant of an immunoreceptor, or a portion thereof, and the antigen-binding molecule is a multispecific antigen-binding molecule having a target antigen recognition site and an immunoreceptor recognition site which recognizes the immunoreceptor.

The present is directed to compositions comprising regulatory T cell epitopes, wherein said epitopes comprise a polypeptide comprising at least a portion of SEQ NOS: 1-73, fragments and/or variants thereof, as well as methods of producing and using the same.

A method of generating a population of genetically modified veto cells is disclosed. The method comprising: (a) providing a population of cells comprising T cells, the T cells comprising at least 40% memory CD8.sup.+ T cells; (b) culturing the population of cells comprising T cells with an antigen or antigens under conditions which allow enrichment of tolerance-inducing antigen-specific cells having a central memory T-lymphocyte (Tcm) phenotype, the cells being depleted of graft versus host (GVH) reactivity; and (c) transducing the cells with a polynucleotide encoding a heterologous cell surface receptor comprising a T cell receptor signaling module, thereby generating the population of genetically modified veto cells.

A method for performing gene editing on a target site in a cell, specifically a method for performing gene editing on a target site of a cell genome, comprising: (a) providing a cell to be genetically edited; (b) introducing into the cell (i) a gene editing enzyme or the encoding nucleic acid thereof or a first expression vector expressing the gene editing enzyme; and (ii) gRNA or a second expression vector expressing the gRNA, and performing gene editing on a target site of the cell genome, the gRNA directing the gene editing enzyme to perform fixed-point cutting on the target site; the targeting sequence of the gRNA targeting comprises one or more of the sequences shown in SEQ ID. No. 1-9. The method enables efficient gene editing to be performed on the target site.

The present disclosure provides compositions and methods for delivering a nucleic acid sequence encoding a chimeric antigen receptor (CAR) to an immune cell using a retroviral vector comprising an optimized Cocal vesiculovirus envelope protein.

The present disclosure relates generally to ex vivo expanded T cell populations suitable for use in adoptive immunotherapy. The disclosure also provides compositions and methods useful for preparing such ex vivo expanded T cell populations, as well as methods for the prevention and/or treatment of health conditions using the disclosed T cell populations.