188 results about "Immune therapy" patented technology

Disclosed herein are chimeric receptors comprising an extracellular domain with affinity and specific for the Fc portion of an immunoglobulin molecule (Ig) (e.g., an extracellular ligand-binding domain of F158 FCGR3A or V158 FCGR3A variant); a transmembrane domain (e.g., a transmembrane domain of CD8α); at least one co-stimulatory signaling domain (e.g., a co-stimulatory signaling domain of 4-1BB); and a cytoplasmic signaling domain comprising an immunoreceptor tyrosine-based activation motif (ITAM) (e.g., a cytoplasmic signaling domain of CD3ζ). Also provided herein are nucleic acids encoding such chimeric receptors and immune cells expressing the chimeric receptors. Such immune cells can be used to enhance antibody-dependent cell-mediated cytotoxicity and/or to enhance antibody-based immunotherapy, such as cancer immunotherapy.

The invention relates to immunotherapeutic compounds and to methods for stimulating an immune response in a subject individual at risk for developing cancer, diagnosed with a cancer, in treatment for cancer, or in post-therapy recovery from cancer or the compounds of the invention can be administered as a prophylactic to a subject individual to prevent or delay the development of cancer.

Described herein are compositions and methods of use of radionuclide-antibody conjugates (for RAIT) and drug-antibody conjugates (ADC). The combination of RAIT and ADC was more efficacious than either RAIT alone, ADC alone, or the sum of effects of RAIT and ADC. The unexpected synergy resulted in decreased tumor growth rate and increased survival, with a high incidence of tumor-free survival in Capan-1 human pancreatic cancer xenografts in nude mice.

The present invention relates to stress proteins and methods of modulating an individual's immune response. In particular, it relates to the use of such stress proteins in immune therapy and prophylaxis, which results in an induction or enhancement of an individual's immune response and as an immunotherapeutic agent which results in a decrease of an individual's immune response to his or her own cells. The present invention also relates to compositions comprising a stress protein joined to another component, such as a fusion protein in which a stress protein is fused to an antigen. Further, the present invention relates to a method of generating antibodies to a substance using a conjugate comprised of a stress protein joined to the substance.

Disclosed are methods for producing fusion proteins with the heterodimeric cytokine, interleukin-12. In order to insure that the proper ratio of fused and non-fused subunits are obtained in the fusion protein, a specific stepwise approach to genetic engineering is used. This consists of first expressing the non-fused p40 IL-12 subunit in a production cell line, followed by or simultaneously expressing in the same cell, a second recombinant fusion protein consisting of the fused polypeptide linked by a peptide bond to the p35 subunit of IL-12. Molecules containing the p35 fusion protein cannot be secreted from the transfected mammalian cell without first complexing in a one to one ratio with the p40 subunit, thus ensuring the production of active heterodimeric fusion proteins.

The present invention provides a combination therapy which relies on a small molecule immune stimulator—cyclic-di-nucleotide (CDN)—that activates DCs via a recently discovered cytoplasmic receptor known as STING (Stimulator of Interferon Genes) formulated with allogeneic human tumor cell lines engineered to secrete high amounts of GM-CSF. This combination therapy can provide an ideal synergy of multiple tumor associated antigens, DC recruitment and proliferation, coupled with a potent DC activation stimulus.

The invention relates to the therapeutic use of stabilized oligoribonucleotides as immune modulatory agents for immune therapy applications. Specifically, the invention provides RNA based oligoribonucleotides with improved nuclease and RNase stability and that have immune modulatory activity through TLR7 and/or TLR8.

Metal-organic frameworks (MOFs) comprising photosensitizers are described. The MOFs can also include moieties capable of absorbing X- rays and/or scintillation. Optionally, the photosensitizer or a derivative thereof can form a bridging ligand of the MOF. Further optionally, the MOF can comprise inorganic nanoparticles in the cavities or channels of the MOF or can be used in combination with an inorganic nanoparticle. Also described are methods of using MOFs and/or inorganic nanoparticles in photodynamic therapy or in X-ray induced photodynamic therapy, either with or without the co-administration of one or more immunotherapeutic agent and/or one or more chemotherapeutic agent.

A method of preparing polysaccharide glassy microparticles which are less than 10 μum in diameter and contain structurally delicate agents, such as proteins, peptides, gene materials, vaccines, antibodies, viruses and liposomes using low-temperature aqueous-aqueous emulsification (free of polyelectrolytes) and freezing-induced phase separation. When delicate agents are added to a polysaccharide-PEG two phase system followed by homogenization (or other shear adding process), the agents partition into the polysaccharide dispersed phase preferentially. These processes help to avoid aggregation of proteins caused by interaction with charged polyelectrolytes used for stabilizing the polysaccharide dispersed phase in our previously reported aqueous-aqueous emulsion. When this system is frozen and lyophilized, glassy particles less than 10 μm in diameter containing delicate agents can be formed. These fine polysaccharide particles protect proteins within their hydrophilic glassy matrix, and can therefore be easily suspended in hydrophobic polymer solutions and formulated to various forms of sustained release devices such microsphere, sheets, fibers, coating layers, and scaffolds. The particles can also be dispersed in hydrophilic gels to improve releasing kinetics and to deliver vaccines and antibodies for immune therapy.

The invention combines a novel combination with two especially important aspects: first, the invention proposes to simultaneously stimulate response in white blood cells and a patient's tumor cells with a mitogen-challenging compound, preferably a lectin, in the preferred mode the selected lectin being phytohemagglutin ("PHA"), and second, to generate heat shock protein. A method of treatment is set out. The method of manufacturing proposed utilizes a system calculated to better insure sterility and streamline production of the cytokine modulator. A method of testing in conjunction with the therapy is also claimed utilizing clinical assessment of disease activity, patient performance status, and quality of life questionnaire. Should efficacy of a treatment fall off, particularly because of mutation or adaption, the composition and method may be re- applied. The invention is not limited to humans, but is also applicable to mammals. The composition is usable as a stand-alone composition, but preferably is used in conjunction with standard therapy such as radiation, chemotherapy or surgery, particularly surgical therapy, and in conjunction with the administration of cystine, as later defined, to enhance immune system competency.

The invention relates to the therapeutic use of novel stabilized oligoribonucleotides as immune modulatory agents for immune therapy applications. Specifically, the invention provides novel RNA-based oligoribonucleotides with improved nuclease and RNase stability and that have immune modulatory activity through TLR7 and/or TLR8.

A medicine for curing alzheimer disease is characterized in that a recombinant virus of gene transfection is regarded as a carrier; the front end of one, two or a plurality of anti A beta single-chain antibody genes is respectively connected with a secretion signal peptide dna sequence; and then the anti A beta single-chain antibody genes are inserted into the recombinant virus gene; finally a packaged product is formed through the recombinant virus. The invention can produce anti A beta single-chain antibody in the body by transfecting the anti A beta single-chain antibody genes capable of prohibiting A beta monomer isomerization and promoting A beta polymer depolymerization on the periphery and in the brains, so as to express scFv in the body for a long time, to effectively remove the A beta in the brains with alzheimer disease, prevent inflammatory reaction of the central nervous system and side effect of capillary bleeding produced in the anti A beta immune therapy, avoid repeated feeding of the anti A beta medicine, and reduce the curing cost. The invention provides a safe and effective novel technology of curing alzheimer disease which works for long and has broad clinical application prospect.

The inventions describes a method for increasing effector T cell accumulation in cancer cell-containing sites of a tumor, comprising administering to a subject in need thereof a pharmaceutically effective amount of an inhibitor of CXCR4 signaling.

The present invention pertains to antigen recognizing constructs against tumor associated antigens (MAGEA1). The invention in particular provides novel T cell receptor (TCR) based molecules which are selective and specific for the tumor expressed antigen of the invention. The TCR of the invention, and TAA binding fragments derived therefrom, are of use for the diagnosis, treatment and prevention of TAA expressing cancerous diseases. Further provided are nucleic acids encoding the antigen recognizing constructs of the invention, vectors comprising these nucleic acids, recombinant cells expressing the antigen recognizing constructs and pharmaceutical compositions comprising the compounds of the invention.

The present invention pertains to antigen recognizing constructs against tumor associated antigens (MAGEA1). The invention in particular provides novel T cell receptor (TCR) based molecules which are selective and specific for the tumor expressed antigen of the invention. The TCR of the invention, and TAA binding fragments derived therefrom, are of use for the diagnosis, treatment and prevention of TAA expressing cancerous diseases. Further provided are nucleic acids encoding the antigen recognizing constructs of the invention, vectors comprising these nucleic acids, recombinant cells expressing the antigen recognizing constructs and pharmaceutical compositions comprising the compounds of the invention.

The invention relates to the field of immunology, more in particular to the field of immune therapy, even more particularly to a method for regulating tolerance to an allergen in a subject and even more specifically, to methods which involve regulation of a glucocorticoid-induced tumor necrosis factor receptor (GITR). Provided is methods of treating allergic disorder and compositions for use therein.

The invention discloses preparation, a variable-region sequence and application of an anti-human programmed death factor 1 (PD-1) monoclonal antibody. The invention provides the anti-human PD-1 monoclonal antibody which comprises gene sequences of heavy-chain variable regions of the monoclonal antibody and gene sequences of light-chain variable regions of the monoclonal antibody. The amino acid sequences of the heavy-chain variable regions are as shown in site 20th to site 134th of SEQ ID NO.3; the amino acid sequences of the light-chain variable regions are shown in site 20th to site 131th of SEQ ID NO.4. The invention discloses the monoclonal antibody 189-H-1 capable of blocking a human PD-1 function and a coding gene thereof. The monoclonal antibody 189-H-1 can be specifically combined with human PD-1 antigen, has median effective concentration EC50 being 1.0667 nM, can specifically block a PD-1/PD-L inhibition signal, and therefore, the monoclonal antibody 189-H-1 can be used as a blocker of a PD-1 access, so that the anti-human PD-1 monoclonal antibody becomes a novel drug for tumor immune therapy, chronic virus infective disease treatment and autoimmune disease treatment.

Methods of inducing T cell proliferation and expansion in vivo for treating conditions wherein antigen-specific T cell immune response are therapeutically desirable such as cancer, infection, inflammation, allergy and autoimmunity and for enhancing the efficacy of vaccines are provided. These methods comprise the administration of at least one CD27 agonist, preferably an agonistic CD27 antibody, alone or in association with another moiety such as immune stimulant or immune modulator such as an anti-CD40, OX-40, 4-IBB, or CTLA-4 antibody or an agent that depletes regulatory cells, or a cytokine. These mono and combination therapies may also optionally include the administration of a desired antigen such as a tumor antigen, an allergen, an autoantigen, or an antigen specific to an infectious agent or pathogen against which a T cell response (often CD8+) is desirably elicited.

An approach combining immune-based therapies with focused radiation, including stereotactic radiation, to treat cancers is disclosed. The use of focused radiation primes the immune system in a similar manner to vaccines to augment immune-based therapies and can counteract the suppressive effects of a tumor. The combination of focused radiation and immune-based therapies, including administration of at least one immunotherapeutic agent, improves survival compared to each therapy alone and can, in some cases, lead to a durable cure. Accordingly, focused radiation can be an adjuvant for immune-based therapies for treating cancers.

Contiguous overlapping peptides (COPs) for the treatment of allergic patients by Specific Immunotherapy (SIT) are provided from the sequence of the major allergens of house dust mites Der p 1 and Der p 2. Such peptides while providing all potential T cell epitopes are devoid of the three dimensional structure of the original allergen, therefore reducing their ability to bind IgE. As a result increased amounts of COPs can be administered per injection, therefore reducing both the number of injections and the length of the immunotherapy treatment.