Provided in the present invention are the preparation for a chimeric antigen receptor immune cell constructed on the basis of a growth arrest-specific protein 6 and the use of the chimeric antigen receptor immune cell. Specifically, provided in the present invention is a chimeric antigen receptor (CAR) based on GAS6 transformation. The CAR contains an extracellular binding domain, which can specifically target a GAS6 receptor. The CAR immune cell of the present invention has a strong specificity and target affinity, thereby also having a strong target cell killing capability and a high safety.

The present disclosure provides a method of treating cancer, comprising administering an anti-LAIR1 antibody to a subject suffering from a cancer that is resistant to checkpoint inhibitor blockade therapy.

Described herein are multicistronic expression systems that encode chimeric proteins, specifically membrane-cleavable chimeric systems and chimeric antigen receptors. Also described herein are nucleic acids, cells, and methods directed to the same.

The present disclosure pertains to a method of construction and use of a novel bispecific chimeric antigen receptor (CAR) within the field of immunotherapy. The CAR described herein comprises an antigen-binding domain, a connecting peptide (C-peptide), a hinge region, a transmembrane domain, a 4-1BB co-stimulatory signaling domain, and a CD3 signaling domain. The antigen-binding domain is composed of either an anti-CD19 scFv and an anti-CD22 nanobody, or an anti-Her2 scFv paired with a ligand capable of recognizing IGF1R. The bispecific CAR-T cell provided by the present disclosure is constructed based on the ligation design involving an antiparallel -stranded loop (BS Loop) linker.

Neuroblastoma (NB) remains a leading cause of childhood cancer morbidity and mortality. Heritable activating mutations are present in the anaplastic lymphoma kinase (ALK) oncogene and these same mutations are frequently somatically acquired during high-risk NB tumorigenesis. ALK has been established as a tractable molecular target in NB and provides the rationale for the clinical development of ALK inhibition therapy. Anti-ALK antibodies and antigen binding fragments thereof are provided along with methods of use thereof.

The disclosure features modified regulatory T (T.sub.REG) cells having increased lineage stability, decreased activation of T cells (e.g., conventional T (T.sub.CONV) cells), and/or increased resistance to immune rejection, and methods of producing and using such cells, for example, in the treatment of graft versus host disease (GVHD).

The disclosure provides synthetic immune receptors (SIRs), nucleic acids encoding the SIRs, methods of making and using the SIRs, in, for example, adoptive cell therapy.

Described herein are compositions and methods for producing regulatory T cells (Tregs) with stable immunosuppressive phenotypes by modifying cells to promote expression of TGFR1, Smad2, and/or Smad3.

The present disclosure relates to anti-glyco-cMET antibodies and antigen binding fragments thereof that specifically bind to a cancer-specific glycosylation variant of cMET and related fusion proteins and antibody-drug conjugates, as well as nucleic acids encoding such biomolecules. The present disclosure further relates to use of the antibodies, antigen-binding fragments, fusion proteins, antibody-drug conjugates and nucleic acids for cancer therapy.

The present disclosure provides modified cell(s), i.e., immune cell(s) or precursor cell(s) thereof, wherein the cell(s) are engineered to express: (a) a first chimeric antigen receptor (CAR) having affinity for CD19, and (b) a second CAR having affinity for a tumor antigen, wherein the tumor antigen is not CD19. Also provided are methods and uses of the modified cells, e.g., for treating at least one sign and/or symptom of cancer in a subject. The modified cells expand in the peripheral blood of the subject. Related nucleic acids, vectors, and pharmaceutical compositions are also provided.