The present disclosure relates to compositions and methods of killing cells. In particular examples, the method includes contacting a cell having a cell surface protein with a therapeutically effective amount of an antibody-IR700 molecule, wherein the antibody specifically binds to the cell surface protein, such as a tumor-specific antigen on the surface of a tumor cell. The cell is subsequently irradiated, such as at a wavelength of 660 to 740 nm at a dose of at least 1 J cm.sup.−2. The cell is also contacted with one or more therapeutic agents (such as an anti-cancer agent), for example about 0 to 8 hours after irradiating the cell, thereby killing the cell. Also provided are methods of imaging cell killing in real time, using fluorescence lifetime imaging. Also provided are wearable devices that include an article of clothing, jewelry, or covering; and an NIR LED incorporated into the article, which can be used with the disclosed methods.

The present disclosure provides methods and compositions for enhancing the immune response toward cancers and pathogens. It relates to chimeric antigen receptors (CARs) comprising a mutated CD28 intracellular motif, and cells comprising such CARs. The presently disclosed subject matter further relates to the use of said cells for treating diseases, e.g., for treating cancers.

The invention provides an isolated and purified nucleic acid sequence encoding a chimeric antigen receptor (CAR) directed against B-cell Maturation Antigen (BCMA). The invention also provides host cells, such as T-cells or natural killer (NK) cells, expressing the CAR and methods for destroying multiple myeloma cells.

The invention provides novel light-switchable CAR T-cells that can be remotely controlled through NIR-light-converting upconvension nanoparticles, and related CAR T constructs, nanoparticles, compositions and methods thereof for optogenetic therapy.

The invention provides monoclonal antibodies and antigen-binding fragments thereof specific for TNFR2, and methods of using the same to treat cancer or autoimmune disorder, including combination therapy with antagonists of the PD-1/PD-L1 immune checkpoint.

The present disclosure provides TGFβ inhibitor therapy for treating immunosuppressive conditions, such as cancer. Selection of suitable therapy and patients who are likely to benefit from such therapy are also disclosed, as well as methods of treating cancer and methods of predicting and monitoring therapeutic response. Related compositions, methods and therapeutic use are also disclosed.

The invention refers to an anti-oxMIF/anti-CD3 antibody comprising at least one binding site specifically recognizing oxMIF and one binding site specifically recognizing CD3, which is an IgG wherein a scFv is fused to only one of the two heavy IgG chains, an IgG wherein one Fab arm is replaced by a bispecific-T-cell-engager (BiTE), or an IgG wherein both Fab arms are replaced by scFvs with different binding specificities, and its use in the treatment of hyperproliferative diseases, specifically in the treatment of cancer.

The present invention relates to antibodies, including humanized antibodies that bind human Microfibrillar-associated protein 4 (MFAP4). The invention also relates to uses of such antibodies.

The present invention relates to antibodies, including humanized antibodies that bind human Microfibrillar-associated protein 4 (MFAP4). The invention also relates to uses of such antibodies.

The invention discloses an antibody that binds an extracellular part of human HVEM on human HVEM-expressing cells, that prevents binding of BTLA to HVEM when the antibody is bound to said extracellular part of HVEM, wherein said antibody displaces BTLA bound to said extracellular part of HVEM. The invention also discloses the use of such an antibody in combating certain diseases.