201 results about "Cell killing" patented technology

A method and pharmaceutical composition are provided for enhancing the endogenous immune response-mediated elimination of a population of pathogenic cells in a host animal wherein the pathogenic cells preferentially express, uniquely express, or overexpress a binding site for a particular ligand. The invention comprises administering the ligand conjugated to an immunogen to a host animal harboring the population of pathogenic cells. Antibodies, preexisting or administered to the host animal to establish a passive immunity, directed against the immunogen bind to the ligand-immunogen conjugate resulting in elimination of the pathogenic cells by the host's immune response. At least one additional therapeutic factor is administered selected from the group consisting of a cell killing agent, a tumor penetration enhancer, a chemotherapeutic agent, antimicrobial agent, a cytotoxic immune cell, and a compound capable of stimulating an endogenous immune response wherein the compound does not bind to the ligand-immunogen conjugate.

The present invention relates to the transient modification of cells. In particular embodiments, the cells are immune systems, such as PBMC, PBL, T (CD3+ and / or CD8+) and Natural Killer (NK) cells. The modified cells provide a population of cells that express a genetically engineered chimeric receptor which can be administered to a patient therapeutically. The present invention further relates to methods that deliver mRNA coding for the chimeric receptor to unstimulated resting PBMC, PBL, T (CD3+ and / or CD8+) and NK cells and which delivers the mRNA efficiently to the transfected cells and promotes significant target cell killing.

The present invention is directed to T-cell epitope delivering polypeptides which deliver one or more CD8+ T-cell epitopes to the MHC class I presentation pathway of a cell, including toxin-derived polypeptides which comprise embedded T-cell epitopes and are de-immunized. The present invention provides cell-targeted, CD8+ T-cell epitope delivering molecules for the targeted delivery of cytotoxicity to certain cells, e.g., infected or malignant cells, for the targeted killing of specific cell types, and the treatment of a variety of diseases, disorders, and conditions, including cancers, immune disorders, and microbial infections. The present invention also provides methods of generating polypeptides capable of delivering one or more heterologous T-cell epitopes to the MHC class I presentation pathway, including polypeptides which are 1) B-cell and / or CD4+ T-cell de-immunized, 2) comprise embedded T-cell epitopes, and / or 3) comprises toxin effectors which retain toxin functions.

Compositions and methods for inducing cell membrane wounding, cell permeabilization and cell killing are provided. The composition comprises a polyvalent agent that binds to a highly expressed cell surface antigen present on the surface of a cell. Preferably, the cell surface antigen is associated with the cytoskeleton of the cell. A preferred polyvalent agent is an IgM, and enhanced cell wounding and killing can be provided by the addition of a crosslinking agent. At sublethal concentrations in vivo, the cell wounding antibodies permeabilize cells and dramatically enhance response to chemotherapeutic agents, even in patients refractory to the chemotherapeutic agents.

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<-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 invention discloses a cryopreservation solution for preserving congenital intrathoracic kidney (CIK) cells and application thereof. The cryopreservation solution for preserving the CIK cells is prepared according to the following methods: adding dimethyl sulfoxide and dextran into a lymphocyte serum-free medium, so that the volume percent content of the dimethyl sulfoxide is 5-15 percent, and the volume percent content of the dextran is 5-15 percent. Compared with the cells before cryopreservation, the cells cryopreserved by employing the cryopreservation solution have the following advantages: (1) the cellular morphology does not have obvious difference; (2) immunophenotype (CD3+CD56+CD8+) does not have obvious difference; and (3) the cell proliferation activity and cell killing activity do not have obvious difference.

The invention relates to a killing cell for high-efficiency and stable expression of antibodies and a use thereof. Specifically, the invention provides the transgenic killing cell; a genome of the killing cell is stably integrated with an expression cassette containing an encoding sequence of human Fc segment-containing antibodies, or containing an encoding sequence of chimeric antigen receptors and inhibitory antibodies or activated type antibodies, and both ends of the expression cassette contain inverted terminal repeated sequences of a transposon. The killing cell can stably express the human Fc segment-containing antibodies or the chimeric antigen receptors and antigen-binding fragments derived from interested antibodies with high level while maintaining cell killing toxic effect. In addition, for preventing systemic toxicity and autoimmune diseases caused by over expression of antibodies due to in-vivo continuous proliferation of immune cells for stable expression of the antibodies, a molecular braking system is also introduced. With use of monoclonal antibody agents appearing on the market, the killing cell integrated with the antibody expression cassette can be quickly eliminated, and the safety of treatment is effectively improved.

A method of killing a specific target cell / tissue is disclosed. The method comprises exposing the specific target cell / tissue to a composition-of-matter comprising a double stranded RNA molecule associated with a targeting moiety selected capable of targeting to the specific target cell / tissue, thereby killing the specific target cell / tissue.

Disclosed herein are methods and compositions for enhancing the cell-killing activity of anti-neoplastic agents by inhibiting the activity of a lysyl oxidase-type enzyme. Also disclosed are methods for screening for chemotherapeutic agents, and for molecules that enhance the activity of chemotherapeutic agents, using cells grown on an extracellular matrix.

The invention provides a composition, and method of use thereof, comprising self-antigen displaying nanoparticles to target auto-reactive immune components for treating and / or preventing the autoimmune diseases associated therewith. The nanoparticles can also be loaded with cytotoxic drugs for targeted cell killing or with immune-tolerizing compounds to normalize the immune regulation.

Compositions and methods for inducing cell membrane wounding, cell permeabilization and cell killing are provided. The composition comprises a polyvalent agent that binds to a highly expressed cell surface antigen present on the surface of a cell. Preferably, the cell surface antigen is associated with the cytoskeleton of the cell. A preferred polyvalent agent is an IgM, and enhanced cell wounding and killing can be provided by the addition of a crosslinking agent. At sublethal concentrations in vivo, the cell wounding antibodies permeabilize cells and dramatically enhance response to chemotherapeutic agents, even in patients refractory to the chemotherapeutic agents.