Abstract:
Human antibodies, preferably recombinant human antibodies, both humanized and chimeric, which specifically bind to human OX40 are disclosed. Preferred antibodies have high affinity for OX40 receptor and activate the receptor in vitro and in vivo. The antibody can be a full-length antibody or an antigen-binding portion thereof. The antibodies, or antibody portions, are useful for modulating receptor activity, e.g., in a human subject suffering from a disorder in which OX40 activity is detrimental. Nucleic acids, vectors and host cells for expressing the recombinant human antibodies are provided, and methods of synthesizing the recombinant human antibodies, are also provided.
Abstract:
Methods, compositions and kits are disclosed for inhibiting interferon production and modulating immune responses, particularly an autoimmune response. In certain embodiments, the methods involve administering an effective amount of a BST2 protein or a nucleic acid encoding an BST2 protein to treat an autoimmune disease or disorder.
Abstract:
Methods, compositions and kits are disclosed for inhibiting interferon production and modulating immune responses, particularly an autoimmune response. In certain embodiments, the methods involve administering an effective amount of a BST2 protein or a nucleic acid encoding an BST2 protein to treat an autoimmune disease or disorder.
Abstract:
OX40L inhibits the generation of IL-10-producing Tr1 cells from naïve and memory CD4+ T cells induced by the immunosuppressive drugs dexamethasone and vitamin D3. This unique function of OX40L is not shared by two other costimulatory TNF-family members, GITR-ligand and 4-1BB-ligand. OX40L also strongly inhibits the generation of IL-10-producing Tr1 cells induced by two physiological stimuli provided by inducible costimulatory ligand and immature DCs and inhibits the production of IL-10 by regulatory T cells. It has thus been shown that signaling the OX40-receptor on human T cells by monoclonal antibodies, small molecules, or OX40L regulates the generation and function of IL-10 producing immunosuppressive T cells. Also provided are high throughput methods for identifying substances that promote or inhibit the generation and function of IL-10 producing T cells. Numerous disease states, such as human allergic, autoimmune, and autoimmune diseases, and cancer, may be treated by targeting OX40/OX40L.
Abstract:
OX40L inhibits the generation of IL-10-producing Tr1 cells from naïve and memory CD4+ T cells induced by the immunosuppressive drugs dexamethasone and vitamin D3. This unique function of OX40L is not shared by two other costimulatory TNF-family members, GITR-ligand and 4-1BB-ligand. OX40L also strongly inhibits the generation of IL-10-producing Tr1 cells induced by two physiological stimuli provided by inducible costimulatory ligand and immature DCs and inhibits the production of IL-10 by regulatory T cells. It has thus been shown that signaling the OX40-receptor on human T cells by monoclonal antibodies, small molecules, or OX40L regulates the generation and function of IL-10 producing immunosuppressive T cells. Also provided are high throughput methods for identifying substances that promote or inhibit the generation and function of IL-10 producing T cells. Numerous disease states, such as human allergic, autoimmune, and autoimmune diseases, and cancer, may be treated by targeting OX40/OX40L.
Abstract:
Human antibodies, preferably recombinant human antibodies, both humanized and chimeric, which specifically bind to human OX40 are disclosed. Preferred antibodies have high affinity for OX40 receptor and activate the receptor in vitro and in vivo. The antibody can be a full- length antibody or an antigen-binding portion thereof. The antibodies, or antibody portions, are useful for modulating receptor activity, e.g., in a human subject suffering from a disorder in which OX40 activity is detrimental. Nucleic acids, vectors and host cells for expressing the recombinant human antibodies are provided, and methods of synthesizing the recombinant human antibodies, are also provided.
Abstract:
Human antibodies, preferably recombinant human antibodies, both humanized and chimeric, which specifically bind to human OX40 are disclosed. Preferred antibodies have high affinity for OX40 receptor and activate the receptor in vitro and in vivo. The antibody can be a full-length antibody or an antigen-binding portion thereof. The antibodies, or antibody portions, are useful for modulating receptor activity, e.g., in a human subject suffering from a disorder in which OX40 activity is detrimental. Nucleic acids, vectors and host cells for expressing the recombinant human antibodies are provided, and methods of synthesizing the recombinant human antibodies, are also provided.
Abstract:
Methods and compositions for treating disease are provided. More particularly, methods and compositions of inhibiting pathogenic interferon production are prevented, which may be useful in the treatment of various diseases. In other embodiments, therapeutic compounds and methods for the treatment of autoimmune diseases and chronic inflammatory diseases are provided. One such method is a method for inhibiting pathogenic interferon production or inhibiting activation of plasmacytoid dendritic cells or treating an autoimmune or chronic inflammatory disease, which comprises inhibiting one or more of LL-37 and hCAP18.
Abstract:
Provided are methods of modulating activity of regulatory T cells, CD4 + T cells, and CD8 + T cells. Also provided are methods of treating immune disorders, infections and cancer. To this end agonists or antagonists of the glucocorticoid-induced tumor necrosis factor receptor (GITR) or its ligand are used.
Abstract:
Methods and compositions for treating disease are provided. More particularly, methods and compositions of inhibiting pathogenic interferon production are prevented, which may be useful in the treatment of various diseases. In other embodiments, therapeutic compounds and methods for the treatment of autoimmune diseases and chronic inflammatory diseases are provided. One such method is a method for inhibiting pathogenic interferon production or inhibiting activation of plasmacytoid dendritic cells or treating an autoimmune or chronic inflammatory disease, which comprises inhibiting one or more of LL-37 and hCAP18.