The present disclosure provides modified immune cells or precursors thereof (e.g. T cells) comprising a first chimeric antigen receptor (CAR) capable of binding human IL13R2, a second CAR capable of binding EGFR or an isoform thereof, and a dominant negative TGF type II receptor (DN-TGFRII). Compositions and methods of treatment are also provided.

The invention relates to polypeptides and chimeric antigen receptors (CARs) comprising an intracellular domain of a Fc alpha Receptor (FcR), a transmembrane domain of a FcR, and a ligand-binding domain, to cells comprising and expressing such polypeptides and CARs and to uses thereof.

Chimeric antigen receptors (CARs) containing HIV envelope antigen binding domains are disclosed. Nucleic acids, recombinant expression vectors, host cells, antigen binding fragments, and pharmaceutical compositions, relating to the CARs are also disclosed. Methods of treating or preventing HIV-infection in a subject, and methods of making CAR T cells are also disclosed. Results of treating or preventing HIV-infection, and results of making CAR T cells are also disclosed.

The present invention relates to methods for universal immune receptor cell based therapies.

The present disclosure provides allogeneic cells that cause reduced risks of graft-versus-host disease (GVHD) and reduced risk of CD8 and NK cell rejections, for example, when used to treat diseases, such as cancer and/or autoimmune disease, in a patient. The allogeneic cells may be genetically engineered to reduce the expression or activity of CD58. Methods of preparing and using such allogeneic cells are also provided.

The present disclosure provides binding-triggered transcriptional switch polypeptides, nucleic acids comprising nucleotide sequences encoding the binding-triggered transcriptional switch polypeptides, and host cells genetically modified with the nucleic acids. The present disclosure also provides chimeric Notch receptor polypeptides, nucleic acids comprising nucleotide sequences encoding the chimeric Notch receptor polypeptides, and host cells transduced and/or genetically modified with the nucleic acids. The present disclosure provides transgenic organisms comprising a nucleic acid encoding a binding triggered transcriptional switch polypeptide and/or a chimeric Notch receptor polypeptide of the present disclosure. Binding triggered transcriptional switch polypeptides and chimeric Notch receptor polypeptides of the present disclosure are useful in a variety of applications, which are also provided.

The invention relates to an inhibitory chimeric antigen receptor (N-CAR) comprising an extracellular domain comprising an antigen binding domain, a transmembrane domain, and, an intracellular domain wherein the intracellular domain comprises an Immunoreceptor Tyrosine-based Switch Motif ITSM, wherein said ITSM is a sequence of amino acid TX.sub.1YX.sub.2X.sub.3X.sub.4, wherein X.sub.1 is an amino acid X.sub.2 is an amino acid X.sub.3 is an amino acid and X.sub.4 is V or

Aspects of the present disclosure are directed to INCENP-targeting polypeptides, including antibodies, antibody-drug conjugates, antibody fragments, antibody-like molecules, and chimeric receptors. Also disclosed herein are nucleic acids encoding for such INCENP-targeting polypeptides and cells comprising such nucleic acids. Described are methods for detection, diagnosis, and treatment of cancer using INCENP-targeting polypeptides.

The present application provides single-domain antibodies targeting BCMA, and chimeric antigen receptors (such as monovalent CAR, and multivalent CAR including bi-epitope CAR) comprising one or more anti-BCMA single-domain antibodies. Further provided are engineered immune effector cells (such as T cells) comprising the chimeric antigen receptors. Pharmaceutical compositions, kits and methods of treating cancer are also provided.

Provided are a chimeric antigen receptor immune cell, and a preparation method therefor and an application thereof. The surface of the chimeric antigen receptor immune cell expresses a receptor targeting a specific antigen, and also expresses a signal conversion protein. The signal conversion protein is a fusion protein containing a dominant negative receptor TGFBR2 extracellular element and an IL-7R intracellular element. The chimeric antigen receptor immune cell can further convert, by means of the signal conversion protein, the inhibitory signal of a TGF- immunosuppressive factor in a tumor microenvironment that is not conducive to the survival of immune cells into a cytokine activation signal, thereby significantly enhancing the survival of the immune cells and having a more sustained tumor killing effect.