124 results about "CD86" patented technology

The present application relates to CTLA4-Ig immunoadhesins that target CD80 and CD86, and their use, particularly for therapeutic purposes.

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 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.

This disclosure provides a multi-specific fusion protein composed of a CD86 antagonist binding domain and another binding domain that is an IL-10 agonist, an HLA-G agonist, an HGF agonist, an IL-35 agonist, a PD-1 agonist, a BTLA agonist, a LIGHT antagonist, a GITRL antagonist or a CD40 antagonist. The multi-specific fusion protein may also include an intervening domain that separates the other domains. This disclosure also provides polynucleotides encoding the multi-specific fusion proteins, compositions of the fusion proteins, and methods of using the multi-specific fusion proteins and compositions.

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.

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.

A method and composition for inducing human dendritic cells to a condition of reduced capacity for antigen-specific activation of T cells, and, in mature dendritic cells, increased production of extracellular IL-10 is disclosed. A population of dendritic cells is exposed to a substantially uncharged antisense compound containing 12-40 subunits and a base sequence effective to hybridize to an expression-sensitive region of a preprocessed or processed human CD86 transcript identified, in its processed form, by SEQ ID NO:33, to form a duplex structure between said compound and transcript having a Tm of at least 45° C. Formation of the duplex blocks expression of full-length CD86 in said cells, which in turn leads to reduced capacity for antigen-specific activation of T cells, and, in mature dendritic cells, increased production of extracellular IL-10.

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 discloses an artificial antigen submitting cell and preparing method, which comprises the following steps: choosing human chronic granular leukocyte leukemia bacterial strain K562 cell as carrier; transfer-dying and expressing eucaryon expressing carrier of CD32a; expressing CD32 molecular on the surface of K562 cell stably through G418 screening and flowed cell sorting device sorting; forming K32 cell; producing eucaryon expressing carrier of double expressing CD86 and 4-1BBL co-simulating signal; proceeding homomycin screen and sort with flowed cell device for the K32 cell; getting stable expression K32 cell of CD86 and 4-1BBL molecule; getting the end product. This invention possesses low cost and good repeatability, which can inhibit die effectively.

The present invention relates to a method for the differentiation and/or maturation of immature myeloid dendritic cells (DC) into HLA-DR, CD86, CD83 and IL12 (p40) dendritic cells comprising incubating said DC with dg T cells; and to a method for the differentiation and/or maturation of immature myeloid dendritic cells (DC) into HLA-DR, CD86, CD83 and IL12 (p70) dendritic cells comprising incubating said DC with activated dg T cells. Specific compositions and uses thereof are described.

The invention discloses a chimeric antigen receptor T (CAR-T) cell as well as a preparation method and application thereof, wherein the CAR of the CAR-T cell comprises a cell membrane exoantigen binding region, a hinge region and an intracellular signal transduction region; the cell membrane exoantigen binding region is chA21scFv for combining with HER2 protein; and the intracellular signal transduction region is CD28-X-ITAM, wherein the X is ICOS, CD137, CD134, CD80 or CD86 costimulatory molecule. The chA21scFv of the CAR-T cell can express anti-HER2 monoclonal antibody, and the HER2 protein is as a target to directly recognize and combine with HER2 protein highly expressed on the surfaces of tumor cells, so that T cells are activated, and cell factors for killing the tumor cells expressing the HER2 protein are secreted.

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.

The invention relates to a kit for combining and analyzing a CD11c+CD11b+DC subgroup and differentiation degree and functions thereof. The kit comprises eight antibodies: CD11c, CD80, CD86, CD11b, HLA-RD, IL-12, IL-23 and IL-27. The invention further provides a method for combining and analyzing a CD11c+CD11b+dendritic cell sub-group and the differentiation degree and functions thereof. With the adoption of the kit and the method, a whole set of data of the CD11c+CD11b+dendritic cell subgroup and the differentiation degree and functions thereof can be detected in one step and similar data does not need to be additionally and tediously tested respectively. By applying a design scheme of the invention, the ratio quantity of a CD11c+CD11b+subgroup in dendritic cells can be obtained and the development, differentiation and mature conditions of the subgroup can also be known; and a function condition of the subgroup can also be known and the effect of rapidly and simply obtaining a whole set of immunology detection data of the CD11c+CD11b+dendritic cell subgroup in one step is realized.

Methods for inducing tolerance to a transplant in a subject are disclosed. The methods comprise administering multiple doses of a therapeutically effective amount of a CD40 antagonist alone or in combination with a CD86 antagonist, wherein the first dose of the antagonist is given before or at the time of transplantation; and administering multiple doses of a therapeutically effective amount of an immunosuppressive drug, wherein the first dose of the immunosuppressive drug is given at least several days after transplantation.