Abstract: A human monoclonal antibody that specifically binds tumor necrosis factor receptor 2 (TNFR2), and a defucosylated form of the antibody, are described. The TNFR2-specific antibody was isolated from a human scFv phage display antibody library. The disclosed antibodies promote antibody-dependent cell-mediated cytotoxicity (ADCC) of human TNFR2+ CD4+ T regulatory cells in a dose- and time-dependent manner. Methods of using the TNFR2 antibodies, such as for tumor immunotherapy, are described.

Abstract: Methods of treating cancer or reducing the incidence of relapse of a cancer in a subject comprising co-administration of Toll-like receptor (TLR) 4 ligand, such as an HMGN1 protein, and a TLR 7 or 8 ligand, and optionally an immune checkpoint inhibitor, to the subject in need of such therapy. The TLR4-mediated immune-stimulating effect is synergistically enhanced by ligands of TLR7 or 8, and the immune checkpoint inhibitor. Also described here is a nanoparticle delivery platform for the co-administration of the TLR 4 ligand and the TLR 7 or 8 ligand.

Abstract: A human monoclonal antibody that specifically binds tumor necrosis factor receptor 2 (TNFR2), and a defucosylated form of the antibody, are described. The TNFR2-specific antibody was isolated from a human scFv phage display antibody library. The disclosed antibodies promote antibody-dependent cell-mediated cytotoxicity (ADCC) of human TNFR2+ CD4+ T regulatory cells in a dose- and time-dependent manner. Methods of using the TNFR2 antibodies, such as for tumor immunotherapy, are described.

Abstract: Methods of treating cancer or reducing the incidence of relapse of a cancer in a subject comprising co-administration of Toll-like receptor (TLR) 4 ligand, such as an HMGN1 protein, and a TLR 7 or 8 ligand, and optionally an immune checkpoint inhibitor, to the subject in need of such therapy. The TLR4-mediated immune-stimulating effect is synergistically enhanced by ligands of TLR7 or 8, and the immune checkpoint inhibitor. Also described here is a nanoparticle delivery platform for the co-administration of the TLR 4 ligand and the TLR 7 or 8 ligand.

Abstract: A method of enhancing an antigen-specific immune response in a host comprising administering to the host an HMGN polypeptide comprising at least one of HMGN1, HMGN3a, HMGN3b, HMGN4, Nsbp1, or a functional fragment thereof, in an amount effective to enhance an antigen-specific immune response; as well as a pharmaceutical composition comprising an HMGN polypeptide comprising at least one of HMGN1, HMGN3a, HMGN3b, HMGN4, Nsbp1, or a functional fragment thereof, and an antigen, or nucleic acids encoding such molecules; and related methods and compositions.

Abstract: A method of enhancing an antigen-specific immune response in a host comprising administering to the host an HMGN polypeptide comprising at least one of HMGN1, HMGN3a, HMGN3b, HMGN4, Nsbp1, or a functional fragment thereof, in an amount effective to enhance an antigen-specific immune response; as well as a pharmaceutical composition comprising an HMGN polypeptide comprising at least one of HMGN1, HMGN3a, HMGN3b, HMGN4, Nsbp1, or a functional fragment thereof, and an antigen, or nucleic acids encoding such molecules; and related methods and compositions.

Abstract: A method of enhancing an antigen-specific immune response in a host comprising administering to the host an HMGN polypeptide comprising at least one of HMGN1, HMGN3a, HMGN3b, HMGN4, Nsbp1, or a functional fragment thereof, in an amount effective to enhance an antigen-specific immune response; as well as a pharmaceutical composition comprising an HMGN polypeptide comprising at least one of HMGN1, HMGN3a, HMGN3b, HMGN4, Nsbp1, or a functional fragment thereof, and an antigen, or nucleic acids encoding such molecules; and related methods and compositions.

Abstract: A method of enhancing an antigen-specific immune response in a host comprising administering to the host an HMGN polypeptide comprising at least one of HMGN1, HMGN3a, HMGN3b, HMGN4, Nsbp1, or a functional fragment thereof, in an amount effective to enhance an antigen-specific immune response; as well as a pharmaceutical composition comprising an HMGN polypeptide comprising at least one of HMGN1, HMGN3a, HMGN3b, HMGN4, Nsbp1, or a functional fragment thereof, and an antigen, or nucleic acids encoding such molecules; and related methods and compositions.

Abstract: A method of enhancing an antigen-specific immune response in a host comprising administering to the host an HMGN polypeptide comprising at least one of HMGN1, HMGN3a, HMGN3b, HMGN4, Nsbpl, or a functional fragment thereof, in an amount effective to enhance an antigen-specific immune response; as well as a pharmaceutical composition comprising an HMGN polypeptide comprising at least one of HMGN1, HMGN3a, HMGN3b, HMGN4, Nsbpl, or a functional fragment thereof, and an antigen, or nucleic acids encoding such molecules; and related methods and compositions.

Abstract: The present invention relates to the discovery that T20/DP178, T21/DP107, and fragments thereof interact with members of the formyl peptide receptor family and thereby modulate cell migration and activation. Novel biological tools, prophylactics, therapeutics and methods of use of the foregoing for modulating an inflammatory response are disclosed.

Abstract: The present invention relates to the discovery of molecules that inhibit viral infection and promote a host immune response to a pathogen. More specifically, the invention disclosed herein concerns molecules that interact with a FPR class receptor, inhibit HIV infection, and stimulate an inflammatory response in a subject. Embodiments of the invention include biotechnological tools, prophylactics, therapeutics, and methods of use of the foregoing, for the study, treatment, and prevention of HIV infection and the induction of an inflammatory response in a subject.

Abstract: The present invention provides a method of enhancing an immune response in a subject, comprising administering an effective amount of LL-37. Moreover, the present invention provides a method of enhancing in a subject an immune response to a vaccine, comprising administering to the subject an effective amount of LL-37 with a vaccine. Further provided is a method of detecting a compound that decreases an immune response in a subject. A method of treating an autoimmune disease in a subject is thus provided. Also provided is a vaccine comprising an immunogen and LL-37.

Abstract: The present invention features methods of inhibiting tumor growth and/or tumor metastasis in a subject, and methods of treating cancer and/or increasing survival of a subject with a tumor, by inhibiting MCP-1 activity in the subject. The present invention also features methods of identifying a compound that inhibits tumor growth or metastasis, by exposing a sample including an MCP-1 polypeptide, an MCP-1 nucleic acid, an MCP-1 receptor polypeptide, or an MCP-1 receptor nucleic acid to a test compound, and detecting a decrease in MCP-1 activity in the sample, wherein a decrease in MCP-1 activity in the sample identifies a compound that inhibits tumor growth or tumor metastasis.

Abstract: The present invention relates to the discovery that T20/DP178, T21/DP107, and fragments thereof interact with members of the formyl peptide receptor family and thereby modulate cell migration and activation. Novel biological tools, prophylactics, therapeutics and methods of use of the foregoing for modulating an inflammatory response are disclosed.

Abstract: The present invention relates to the discovery of molecules that inhibit viral infection and promote a host immune response to a pathogen. More specifically, the invention disclosed herein concerns molecules that interact with a FPR class receptor, inhibit HIV infection, and stimulate an inflammatory response in a subject. Embodiments of the invention include biotechnological tools, prophylactics, therapeutics, and methods of use of the foregoing, for the study, treatment, and prevention of HIV infection and the induction of an inflammatory response in a subject.

Abstract: The present invention relates to the discovery that serum amyloid A (SAA) is a ligand for the FPRL1 receptor. Disclosed herein, are novel biological tools for the study of SAA/FPRL1 complex assembly and prophylactics, therapeutics, and methods of use of the foregoing, which modulate the association of SAA with FPRL1 and thereby effect responses including, but not limited to, signal transduction, chemotaxis, leukocyte migration, immune system response, amyloidosis, inflammatory response, infection, organ rejection, arthritis, atherosclerosis, and neoplasia.

Abstract: A method of using a ureido derivative of a poly-4-amino-2-carboxy-1-methyl pyrrole or a pharmaceutically acceptable salt thereof to inhibit inflammation, particularly non-TNF-&agr; dependent inflammation, in a mammal.

Abstract: The present invention provides a method of enhancing an immune response in a subject, comprising administering an effective amount of LL-37. Moreover, the present invention provides a method of enhancing in a subject an immune response to a vaccine, comprising administering to the subject an effective amount of LL-37 with a vaccine. Further provided is a method of detecting a compound that decreases an immune response in a subject. A method of treating an autoimmune disease in a subject is thus provided. Also provided is a vaccine comprising an immunogen and LL-37.