169 results about "CD80" patented technology

Disclosed herein are compositions and methods of use comprising combinations of anti-CD22 antibodies with a therapeutic agent. The therapeutic agent may be attached to the anti-CD22 antibody or may be separately administered, either before, simultaneously with or after the anti-CD22 antibody. In preferred embodiments, the therapeutic agent is an antibody or fragment thereof that binds to an antigen different from CD22, such as CD19, CD20, CD21, CD22, CD23, CD37, CD40, CD40L, CD52, CD80 and HLA-DR. However, the therapeutic agent may an immunomodulator, a cytokine, a toxin or other therapeutic agent known in the art. More preferably, the anti-CD22 antibody is part of a DNL complex, such as a hexavalent DNL complex. Most preferably, combination therapy with the anti-CD22 antibody or fragment and the therapeutic agent is more effective than the antibody alone, the therapeutic agent alone, or the combination of anti-CD22 antibody and therapeutic agent that are not conjugated to each other. Administration of the anti-CD22 antibody and therapeutic agent induces apoptosis and cell death of target cells in diseases such as B-cell lymphomas or leukemias, autoimmune disease or immune dysfunction disease.

The present invention provides a composition comprising an agent which specifically blocks interaction between B7-H1 and CD80 but not interaction between B7-H1 and PD-1 and a vaccine, optionally in a pharmaceutically acceptable carrier. Further provided is a method of treating or inhibiting abnormal cell proliferation or a viral infection in a host comprising the step of administering an agent which specifically blocks interaction between B7-H1 and CD80 but does not block interaction between B7-H1 and PD-1 in combination with a vaccine against the cancer to a host in need thereof.

The present invention provides compositions comprising one or more RNAi agents (e.g., siRNAs, shRNAs, or RNAi vectors) for the treatment of conditions and diseases mediated by (e.g., featuring IgE-mediated hypersensitivity), as well as systems for identifying RNAi agents effective for this purpose. The compositions are suitable for the treatment of allergic rhinitis and / or asthma. In certain embodiments of the invention the RNAi agent is targeted to a transcript that encodes a protein selected from the group consisisting of the FCεRIα chain, the FCεRIβ chain, c-Kit, Lyn, Syk, ICOS, OX40L, CD40, CD80, CD86, Re1A, Re1B, 4-1BB ligand, TLR1, TLR2, TLR3, TLR4, TLR5, TLR6, TLR7, TLR8, TLR9, CD83, SLAM, common γ chain, and COX-2. In addition, the invention provides RNAi agent / delivery agent compositions and methods of use. In certain embodiments of the invention compositions comprising an RNAi agent are delivered by the respiratory route.

The present invention is directed to methods and kits based, at least in part, on the identification of allele-specific responsiveness or non-responsiveness to glatiramer acetate for the treatment of immune disorders, such as relapsing-remitting multiple sclerosis. The allele-specific responsiveness or non-responsiveness is based on polymorphisms in the following genes, CTSS, MBP, TCRB, CD95, CD86, IL-1R1, CD80, SCYA5, MMP9, MOG, SPP1 and IL-12RB2.

It has been found that dendritic cells can be prepared which cannot mature. These cells can provide signal 1 to T cells but cannot provide co-stimulatory signal 2. T cells which are stimulated by the permanently immature dendritic cells therefore anergise, so the dendritic cells are tolerogenic rather than immunogenic. The cells are generally CD40−ve, CD80−ve and CD86−ve, and remain so when stimulated by inflammatory mediators such as lipopolysaccharide. The cells can be prepared conveniently by the culturing adherent embryonic stem cells in the presence of GM-CSF.

The present invention relates to the identification of molecules, which are specific to CD80 and CD86 antigens. Also preferably, such antibodies are capable of inhibiting the binding of CD28 and CTLA4 to those receptors. Those molecules are able to inhibit T cell mediated immune reactions.

The present invention provides soluble CTLA4 mutant molecules which bind with greater avidity to the CD80 and / or CD86 antigen than wild type CTLA4 or non-mutated CTLA4Ig. The soluble CTLA4 molecules have a first amino acid sequence comprising the extracellular domain of CTLA4, where certain amino acid residues within the S25-R33 region and M97-G107 region are mutated. The mutant molecules of the invention may also include a second amino acid sequence which increases the solubility of the mutant molecule.

AS-oligonucleotides are delivered in microsphere form in order to induce dendritic cell tolerance, particularly in the non-obese-diabetic (NOD) mouse model. The microspheres incorporate antisense (AS) oligonucleotides. A process includes using an antisense approach to prevent an autoimmune diabetes condition in NOD mice in vivo and in situ. The oligonucleotides are targeted to bind to primary transcripts CD40, CD80, CD86 and their combinations.

The present invention relates to a transplant rejection in an animal suppressed by administration of an antibody directed at a cell surface antigen selected from the group consisting of CD4, CD8, CD154, LFA-1, CD80, CD86 and ICAM-1, preferably an anti-CD4 antibody, together with a non-cellular protein antigen to generate in the animal a population of regulatory T-lymphocytes; reactivating said population of regulatory T-lymphocytes by further administration to the animal of the non-cellular protein antigen; and transplanting said organ or tissue whilst said population of regulatory T-lymphocytes is activated. Regulatory T cells can be generated ex vivo by culturing T cells with an antibody directed at a cell surface antigen selected from the group consisting of CD4, CD8, CD154, LFA-1, CD80, CD86 and ICAM-1, in the presence of cells that present either alloantigen or a non-cellular protein antigen. Ex vivo generated T-lymphocytes can be used as an alternative method of overcoming transplant rejection or in combination with the in vivo method. A similar approach can be adopted for the treatment of autoimmune conditions.

The present invention is directed to methods and kits based, at least in part, on the identification of allele-specific responsiveness or non-responsiveness to glatiramer acetate for the treatment of autoimmune disorders, such as relapsing-remitting multiple sclerosis. The allele-specific responsiveness or non-responsiveness is based on polymorphisms in the following genes, CTSS, MBP, TCRB, CD95, CD86, IL-1R1, CD80, SCYA5, MMP9, MOG, SPP1 and IL-12RB2.

In this invention, the inventor discloses that naturally occurring IgM anti-lymphocyte antibodies bind to chemokine and non-chemokine receptors on lymphocytes and other cells, and downmodulate certain receptors including CD4 and CD2 on T cells and CD80 and CD86 on macrophages. The inventor also discloses that such antibodies (i) inhibit HIV-1 and other viruses from infecting cells (ii) inhibits activation and proliferation of T lymphocytes (iii) inhibits cytokine and chemokine production (iv) inhibits inflammatory processes, and (v) enhances death of malignant cells. This art or invention is novel in that the antibodies described herein are “naturally occurring” i.e. develop in absence of deliberate immunization and secondly these antibodies are distinct from disease causing autoantibodies in that these naturally occurring antibodies are polyreactive with low binding affinity.

The present invention provides use of soluble CTLA4 mutant molecules which bind with greater avidity to the CD80 and / or CD86 antigen than wild type CTLA4 or non-mutated CTLA4Ig in the treatment of immune disorders associated with graft transplantation.

The invention provides an artificial antigen presenting cell as well as a preparation method and an application thereof. Wherein the artificial antigen presenting cell expresses membrane proteins MICA, IL-12 and CD80, the artificial antigen presenting cell is used for culturing NK cells or peripheral blood mononuclear cells containing the NK cells, the number of the NK cells can be remarkably increased, the service life of the NK cells is prolonged, the activity of the NK cells is improved, and compared with an existing artificial antigen presenting cell for expressing MICA, the artificial antigen presenting cell has a stronger effect of amplifying and activating the NK cells.

Polynucleotides encoding at least one immunizing antigen whose expression is controlled by a promoter derived from a gene encoding a co-stimulatory molecule are provided. The polynucleotides may also encode adjuvants. Compositions comprising at least one immunizing agent and at least one cytokine that enhance dendritic cell stimulation and / or survival are also provided. Methods for eliciting an immune response against the immunizing agent are also provided. The method includes the steps of administering the polynucleotides and, optionally, co-administering an adjuvant.

Compositions comprising CD80-targeted therapeutics and methods of using these compositions are provided for the treatment of a disease or disorder in which CD80-expressing cells or regulatory T cell function contribute to or exacerbate the associated pathology.

The present invention provides a fusion protein capable of blocking a PD-1 / PD-L1 signaling conduction pathway and activating T cells. The fusion protein comprises (i) an antigen-binding fragment derived from an anti-PD-1 antibody and / or an anti-PD-L1 antibody; (ii) an immunoglobulin Fc domain; and (iii) a CD80 extracellular domain (ECD). The present invention also provides a polynucleotide encoding the fusion protein, a vector comprising the polynucleotide, a host cell comprising the polynucleotide or vector, and a use of the fusion protein in individual treating, preventing and / or diagnosingdiseases related with PD-1 / PD-L1 signaling pathway activation and T cell function inhibition.

The invention belongs to the technical field of medicine and relates to a use of cyclic dinucleotide cGAMP and its derivatives as immunologic adjuvants. The study result shows that cGAMP and its derivatives can stimulate the innate immunity of the human body, are effective immunomodulators, can significantly improve the immune response and antibody titer, can stimulate expression of immature dendritic cell surface histocompatible complex MHCII antigens and an enhancement molecule CD80 / CD86, can increase secretion of cytokines and chemokines (such as interleukin and interferon), and can activate and enhance dendritic cells and T cells. Therefore, cGAMP and its derivatives can be used as potential immunologic adjuvants and play an important role in preparation of vaccines.

A chimeric protein expressed from a transgene tranduced into a mammalian tumor cell and method of using the chimeric protein for cancer treatment. The chimeric protein comprises an effector and an anchor, which are linked by a spacer. The chimeric protein, when expressed and exposed on the tumor cell surface in vivo can activate T cells, which further lead to lysis of the tumor cells. The anti-tumor effects can be enhanced by co-expression of certain co-stimulators, such as CD80 or CD86.

The present invention provides soluble CTLA4 mutant molecules which bind with greater avidity to the CD80 and / or CD86 antigen than wild type CTLA4 or non-mutated CTLA4Ig. The soluble CTLA4 molecules have a first amino acid sequence comprising the extracellular domain of CTLA4, where certain amino acid residues within the S25-R33 region and M97-G107 region are mutated. The mutant molecules of the invention may also include a second amino acid sequence which increases the solubility of the mutant molecule.

The choline salt of the CD80 antagonist compound 4-(6-fluoro-3-oxo-1,3-dihydro-pyrazolo[4,3-c]cinnolin-2-yl)-N-(2,2-difluoro-ethyl)-benzamide (I) has good aqueous solubility and is therefore convenient for pharmaceutical use.

A peptide according to the present invention can perform a function identical or similar to the function of natural CTLA-4 and has an excellent degree of skin penetration due to a small size. The peptide according to the present invention effectively binds to antigen presenting cell surface proteins (CD80 and CD86) to inhibit activity of T cells and thus is capable of inhibiting the expression of inflammatory cytokines (for example, IL-2 and IFN-γ). As a result, a composition comprising the peptide according to the present invention exhibits excellent effects in terms of preventing, treating, or improving Th1-mediated immune diseases. Therefore, the superior activity and stability of the peptide according to the present invention can be useful when applied to medicine, quasi-drugs, and cosmetics.