An immunoresponsive cell, such as a T-cell expressing (i) a second generation chimeric antigen receptor comprising: (a) a signalling region; (b) a co-stimulatory signalling region; (c) a transmembrane domain; and (d) a binding element that specifically interacts with a first epitope on a target antigen; and (ii) a chimeric costimulatory receptor comprising (e) a co-stimulatory signalling region which is different to that of (b); (f) a transmembrane domain; and g) a binding element that specifically interacts with a second epitope on a target antigen.

This arrangement is referred to as parallel chimeric activating receptors (pCAR). Cells of this type are useful in therapy, and kits and methods for using them as well as methods for preparing them are described and claimed.

This disclosure relates to therapeutics containing IL-37, chimeric antigen receptors, nucleic acids, or vectors encoding the same. In certain embodiments, this disclosure relates to methods of treating cancer comprising administering a nucleic acid or vector encoding interleukin-37 to a subject diagnosed with cancer and administering T cells expressing a chimeric antigen receptor to the subject. In certain embodiments, this disclosure relates to methods of treating cancer comprising administering a nucleic acid or vector encoding interleukin-37 and a chimeric antigen receptor to a subject diagnosed with cancer.

The present disclosure relates to compositions and methods for enhancing infiltration of lymphocytes into tumor tissue, enhancing anti-tumor lymphocyte activities in tumor microenvionment (TME), inhibiting regulatory lymphocyte (e.g., B and T cells) activities in TME, and/or long term benefit of cell therapies. For example, in a method of in vivo cell expansion, the method comprises administering an effective amount of cells comprising an antigen binding molecule to a subject; and administering an effective amount of presenting cells expressing a solid tumor antigen that the binding molecule binds.

A method for producing CAR-M1 macrophages expressing a chimeric antigen receptor in vitro and in vivo includes using a conjugate of a non-viral gene delivery system and a chimeric antigen receptor gene. The CAR-M1 macrophages are produced in vivo by delivering genes encoding a chimeric antigen receptor and IFN-?, specifically to macrophages in the body, and thus does not require culturing and preparing an in-vitro cellular therapeutic agent, thus reducing the manufacturing costs of therapeutic agents. The CAR-M1 macrophages are a safer therapy since a non-viral vector is used, as compared to the production of CAR-M1 macrophages by gene delivery using a viral vector, and are a novel therapeutic candidate having the advantage of high anticancer efficiency for solid cancers, due to CAR-M1 macrophages in which intrinsic properties of macrophages infiltrating solid cancers and cancer cell phagocytosis are improved.

Provided are methods of inducing differentiation and/or proliferation of T cells and uses thereof. In the present method, peripheral blood mononuclear cells (PBMCs) isolated from a subject are cultivated with bi-specific antibodies (BsAbs) in a culture medium so as to differentiate the PBMCs into the T cells. Each of the T cells has an anti-tumor antigen moiety and an anti-CD3 moiety on its surface. Also provided are methods and pharmaceutical kits for treating subjects suffering from cancers.

Provided is an antibody targeting CLDN18.2. The antibody targeting CLDN118.2 comprises VL and/or VH; the VL comprises the following CDR sequences: a VL CDR1 amino acid sequence as shown in SEQ ID NO: 11 or SEQ ID NO: 12; a VL CDR2 amino acid sequence as shown in SEQ ID NO: 13; and a VL CDR3 amino acid sequence as shown in SEQ ID NO: 14; and the VH comprises the following CDR sequences; a VH CDR1 amino acid sequence as shown in SEQ ID NO: 15; a VH CDR2 amino acid sequence as shown in SEQ ID NO: 16; and a VH CDR3 amino acid sequence as shown in SEQ ID NO: 17. Further disclosed are a bispecific antibody targeting CLDN18.2, a conjugates of the antibody, a CAR molecule targeting CLDN18.2 and a cell comprising same, and applications thereof.

The present invention relates to genetically modified B cells and their uses thereof, for example, for the treatment of a variety of diseases and disorders, including cancer, heart disease, inflammatory disease, muscle wasting disease, neurological disease, and the like. In certain embodiments, the invention relates to an isolated modified B cell (CAR-B cell), capable of expressing a chimeric receptor (CAR-B receptor), wherein said chimeric receptor comprises (a) an extracellular domain; (b) a transmembrane domain; and (c) a cytoplasmic domain that comprises at least one signaling domain. In various embodiments, the invention comprises an isolated modified B cell, wherein said B cell is capable of expressing and secreting a payload, wherein the payload is not naturally expressed in a B cell or is expressed at higher levels than is naturally expressed in a B cell. In various embodiments, the payload is an antibody or fragment thereof.

The present disclosure relates to chimeric Tim4 receptors, host cells modified to include chimeric Tim4 receptor molecules, and methods of making and using such receptor molecules and modified cells.

The present disclosure relates to chimeric Tim4 receptors, host cells modified to include chimeric Tim4 receptor molecules, and methods of making and using such receptor molecules and modified cells.

Provided herein are methods employing various fusion constructs in T cell therapy. The fusion constructs allow for one to reduce, to the point of full removal if desired, the use of IL-2 that would otherwise accompany an in vivo T cell therapy.