The present disclosure relates to treating a subject comprising administering to the subject a therapy (e.g., a cell therapy, e.g., an adoptive cell therapy, e.g., a CAR-T cell therapy), wherein, prior to the administration, the subject has been preconditioned with a personalized amount of a chemotherapeutic agent. The personalized amount provides an optimal exposure to the chemotherapeutic agent.

The present application provides an anti-CD5 antibody. The present application further provides a chimeric antigen receptor (CAR) that specifically binds to a CD5 protein, which comprises a CD5 binding domain, a transmembrane domain, a co-stimulatory domain and an intracellular signaling domain. Further provided are engineered immune effector cells (such as T-cells) comprising the chimeric antigen receptor. The present application further provides use of the CAR and the engineered immune effector cells in the treatment of diseases or conditions associated with the expression of CD5.

The invention relates to nucleic acid constructs comprising a combination of a first sequence encoding a CAR and second sequence encoding an amino acid transporter, and to cells comprising such nucleic acid constructs. It also relates to methods of manufacturing said cells, and to pharmaceutical compositions comprising said nucleic acid constructs or cells, for use in the treatment of diseases with cellular amino-acid depletion such as cancer.

An engineered immune cell comprising a first functional exogenous receptor capable of binding and depleting natural killer (NK) cells, and a second functional exogenous receptor, wherein the engineered immune cell has reduced MHC I on cell surface.

The present invention relates to a novel T-cell receptor binding to MR1, and a use thereof. Unlike a conventional customized anticancer immune T cell therapeutic agent, which are limitedly used depending on cancer type and the expression of cancer antigens according to human leukocyte antigen (HLA) type, T cells in which a T-cell receptor is expressed can be applied to all types of cancer regardless of HLA type.

Provided are a preparation method and an application of CD7-CAR-T cells. The method comprises: (i) providing a sample to be processed containing T cells, (ii) sorting and activating the T cells contained in the sample, so as to obtain activated T cells, (iii) introducing a first viral vector for expressing a CD7 blocking molecule into the activated T cells, so as to obtain CD7 blocked T cells, and (iv) introducing a second viral vector for expressing a CD7-CAR into the CD7-blocked T cells to obtain CD7-CAR-T cells. By adjusting the transfection sequence and transfection time of the lentivirus expressing the CD7 blocking molecule and the lentivirus expressing the CD7-CAR, transfection efficiency is improved, and the cytotoxicity of the CAR-T cells is enhanced.

The compositions and methods described herein are directed to treating solid tumor using CAR T therapy. For example, the compositions include CAR T cells comprising an extracellular domain that binds FCR1, MSLN, GPC-3, ALPP, CD70, CLDN6, ROR1, CD205, ACPP, ADAM12, or CLDN18.2.

The disclosure relates to chimeric antigen receptors and immune effector cells bearing chimeric antigen receptors (CARs). Disclosed herein are improved CARs that are able to recruit Lck and/or and PLC without the need to express CD2, thereby providing efficient CAR function without the risk of CD2-induced fratricide; optionally, the CARs also comprise CD132. Further disclosed herein are improved CARs specific for CD2. Further disclosed herein are improved immune effector cells bearing such improved CARs, therapeutic compositions comprising such improved immune effector cells, and methods for treating cancer using such improved immune effector cells and/or therapeutic compositions.

Provided herein are gRNA comprising a targeting domain that targets CD7, which may be used, for example, to make modifications in cells. Also provided herein are methods of genetically engineered cell having a modification (e.g., insertion or deletion) in the CD7 gene and methods involving administering such genetically engineered cells to a subject, such as a subject having a hematopoietic malignancy.

Disclosed herein are polypeptides, such as monoclonal antibodies (mAbs) and functional fragments thereof, synthetic antigen-binding proteins such as single-chain variable fragments (scFvs), and chimeric antigen receptors (CARs), that can specifically recognize tumor-associated antigens (TAAs) on cancer cells, for example those that express CD33, FLT3, and CLL-1, useful in the treatment of diseases such as cancer.