Abstract: Novel methods and compositions are provided for inhibiting interactions between human immunodeficiency viruses (HIVs) and viral coreceptors, including CXCR4 and/or CCR5 coreceptors. The anti-coreceptor binding agent includes a novel peptide portion of the gp120 envelope protein of HIV-1, as well as peptide analogs and mimetics of this peptide, that specifically binds to, or modulates activity of, the coreceptors(s). The anti-coreceptor binding agent is useful as a prophylactic or therapeutic treatment to prevent or inhibit HIV binding to a susceptible cell and thereby reduces infection and/or moderates or treats related diseases. In alternative embodiments, the peptides, analogs and mimetics are effective to inhibit direct co-receptor binding by HIV virus, coreceptor binding by HIV gp120 proteins or peptides, HIV fusion with target host cells, HIV virion entry into host cells, HIV replication, and HIV transmission between cells and hosts.

Abstract: The present invention relates, e.g., to a method for identifying a peptide of CaG, or an active variant thereof, that modulates a CaG-FPR response (e.g., chemotaxis), comprising screening a candidate CaG peptide or active variant thereof for its ability to modulate a CaG-FPR induced response. Methods for identifying peptide mimetics of CaG, peptides that are more potent agonists of FPR than is CaG, and antagonists of FPR are described.

Abstract: The invention provides compositions and methods of enhancing an immune response in a subject. The compositions comprise eosinophil derived-neurotoxin (EDN) and/or human pancreatic ribonuclease (hPR), which can be used as adjuvants to elicit an enhanced immune response in a subject.

Abstract: The invention relates to the discovery that amyloid ? is a ligand for FPR class receptors, which mediate the inflammation associated with Alzheimer's disease.

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: An isolated, synthetic preparation of a novel neutrophil-specific chemotactic factor (NCF), monoclonal antibodies having specific binding affinity for NCF and a clone containing the complete cDNA coding sequence for NCF are disclosed.

Abstract: An isolated, synthetic preparation of a novel neutrophil-specific chemotactic factor (NCF), monoclonal antibodies having specific binding affinity for NCF and a clone containing the complete cDNA coding sequence for NCF are disclosed.

Abstract: An isolated, synthetic preparation of a novel neutrophil-specific chemotactic factor (NCF), monoclonal antibodies having specific binding affinity of NCF and a clone containing the complete cDNA coding sequence for NCF are disclosed.

Abstract: An isloated, synthetic preparation of a novel neutrophil-specific chemotactic factor (NCF), monoclonal antibodies having specific binding affinity for NCF and a clone containing the complete cDNA coding sequence for NCF are disclosed.

Abstract: The present invention relates to an isolated, synthetic preparation of a novel neutrophil-specific chemotactic factor (NCF), monoclonal antibodies having specific binding affinity for NCF and a clone containing the complete coding sequence for NCF.

Abstract: An isolated, synthetic preparation of a novel neutrophil-specific chemotactic factor (NCF), monoclonal antibodies having specific binding affinity for NCF and a clone containing the complete cDNA coding sequence for NCF are disclosed.