Abstract: The subject invention pertains to agonist peptides of type I interferons and methods of using the peptides. These peptides are based on the amino acid sequence of the C-terminus region of the type I IFN molecules and are capable of binding to the cytoplasmic domain of type I IFN receptors. Surprisingly, these peptides were found to possess the same or similar biological activity as that associated with the full-length, mature type I IFN proteins, even though these peptides do not bind to the extracellular domain of the type I IFN receptors. In one embodiment, the peptide is a peptide of IFN?. In another embodiment, the peptide is a peptide of IFN?. Exemplified peptides of the invention include those having SEQ ID NO:1, SEQ ID NO:2, SEQ ID NO:3, SEQ ID NO:4, SEQ ID NO:5, SEQ ID NO:6, SEQ ID NO:38, SEQ ID NO:39, and SEQ ID NO:40. The subject peptides have been shown to effect increased resistance to viral infection.

Abstract: For determining the presence and amount of human interleukin 3 (IL-3) in a sample, the present invention provides a diagnostic method, wherein an anti-IL-3-antibody, fragment or construct thereof is added to said sample under conditions which allow for binding said antibody, fragment or construct thereof to IL-3 and detecting the amount of antibody bound IL-3 in said sample, wherein the anti-IL-3-antibody is clone 13. Further subject matter of the present invention are the novel antibody clone 13, a nucleic acid encoding said antibody and a hybridoma cell line which produces antibody clone 13. A diagnostic assay kit contains all necessary reagents and materials for performing such assay, preferably an ELISA assay and especially preferably contains antibody clones 13 and 11.

Abstract: The present invention relates to an anti-CSF-1R antibody and binding fragments thereof, DNA encoding the same, host cells comprising said DNA and methods of expressing the antibody or binding fragment in a host cell. The present invention also extends to pharmaceutical compositions comprising the antibody or a binding fragment thereof and use of the antibody, binding fragment and compositions comprising the same in treatment.

Abstract: Broadly neutralizing interferon-? and interferon-? antibody antagonists, polynucleotides encoding the antibodies or fragments, and methods of making and using the foregoing are useful in the treatment of diseases associated with increased production of IFN? and IFN?.

Abstract: Pro-apoptotic agents such as ligands and agonists of agonistic TRAIL receptors can induce or increase apoptosis of cells that cause fibrosis and underlying diseases such as liver, pancreatic, lung and skin diseases characterized by fibrosis, cirrhosis, or complications thereof. The compositions and methods can be used to selectively remove activated hepatic stellate cells (HSCs), the originators of liver fibrosis and cirrhosis, and activated pancreatic stellate cells (PSCs), the originators of pancreas fibrosis and pancreatitis, and can be effective to reduce or prevent further chronic fibrosis by simultaneously reducing multiple fibrosis-associated molecules secreted or induced by such activated stellate cells. The compositions are typically effective to target agonistic TRAIL receptors such as TRAIL-R1/DR4 and TRAIL-R2/DR5 that are selectively expressed in activated HSCs and PSCs in physiological conditions.

Abstract: Methods of treating peripheral vascular disease comprising administering a protein solution site of a defect at least two proteins from the group IL-1ra, sTNF-RI, sTNF-RII, IGF-I, EGF, HGF, PDGF-AB, PDGF-BB, VEGF, TGF-?1, and sIL-1RII. The solution may also comprise white blood cells, platelets, concentrated bone marrow aspirate, and combinations thereof.

Abstract: Methods and therapeutic compositions for treating respiratory diseases, such as chronic obstructive pulmonary disease (COPD) and devices for administering the therapeutic compositions. Methods for treatment include producing a protein solution, producing a concentrated bone marrow aspirate (cBMA), optionally combining the protein solution and cBMA to form an therapeutic composition, and optionally saturating the autologous therapeutic composition with hydrogen gas, and administering the therapeutic composition to a subject in need thereof. The present methods, compositions and devices are useful for treating COPD and the progression of COPD.

Abstract: This disclosure relates to a modified ?-helical bundle cytokine, with reduced activity via an ?-helical bundle cytokine receptor, wherein the ?-helical bundle cytokine is specifically delivered to target cells. Preferably, the ?-helical bundle cytokine is a mutant, more preferably it is a mutant interferon, with low affinity to the interferon receptor, wherein the mutant interferon is specifically delivered to target cells. The targeting is realized by fusion of the modified ?-helical bundle cytokine to a targeting moiety, preferably an antibody. This disclosure relates further to the use of such targeted modified ?-helical bundle cytokine to treat diseases. A preferred embodiment is the use of a targeted mutant interferon, to treat diseases, preferably viral diseases and tumors.

Abstract: Provided are formulations for proteins to be injected into mammals. Specifically, formulations for recombinant IL-12 in mice and primates.

Abstract: This disclosure generally relates to antibodies or antibody fragments which specifically bind to M-CSF. In particular antibodies and antibody fragments are disclosed which bind to M-CSF and which inhibit binding of M-CSF to the M-CSF receptor with an IC50 of 10 pM or less. The invention also relates to nucleic acids, vectors and host cells capable of expressing the antibodies or fragments thereof of the invention, pharmaceutical compositions comprising the antibodies or fragments thereof and uses of said antibodies or fragments thereof and compositions for treatment of specific diseases.

Abstract: An interferon composition is provided for enhancing the platelet count, reducing the recurrence rate of hepatitis, and/or improving the social function of hepatitis patients. The method comprises administering a low dose of IFN (about 5 IU to about 2500 IU of IFN-alpha) to a patient in need thereof. In one embodiment the IFN is alpha IFN or beta IFN, and more particularly, in one embodiment the administered biologically active IFN is human alpha IFN.

Abstract: The present invention relates to a method for obtaining recombinant granulocyte-colony stimulating factor (G-CSF), comprising at least one cation exchange chromatography and at least one hydrophobic interaction chromatography, wherein said two chromatographic steps are immediately consecutive in optional order. In particular, the present invention relates to a method for purifying G-CSF from a mixture of G-CSF and other proteins, comprising two cation exchange chromatography steps which are conducted before and after a hydrophobic interaction chromatography, respectively.

Abstract: In various embodiments chimeric moieties (constructs) are provided that show significant efficacy against cancers. In certain embodiments the constructs comprise a targeting moiety that specifically binds CD138 attached to an interferon or to a mutant interferon. In certain embodiments, the constructs comprise anti-CD138 antibody attached to an interferon alpha (IFN-?) or to a mutant interferon alpha.

Abstract: A method for preventing or treating a cancer includes administering an anti-cancer pharmaceutical composition including an interferon alpha or a polymer conjugate thereof. The pharmaceutical composition can be co-administered with anti-cancer agents. The interferon alpha conjugate shows a longer in vivo half-life and a more excellent anti-cancer activity than the conventional interferon alpha, and in particular, its co-administration with an anti-cancer agent such as gemcitabine has synergistic inhibitory effects on cancer cell growth and proliferation so as to exhibit a remarkably excellent anti-cancer activity. Further, the anti-cancer pharmaceutical composition has excellent in vivo half-life and anti-cancer activity to greatly reduce administration frequency.

Abstract: The field of the present invention relates to genetically engineered fusion molecules, methods of making said fusion molecules, and uses thereof for treatment of autoimmune diseases. More specifically, the present invention provides novel genetically engineered fusion molecules comprising an interferon (IFN) molecule attached to an antibody (Ab) which targets an antigen which is differentially expressed or up-regulated on activated T cells as compared to resting T cells, wherein the fusion molecule when contacted to an activated T cell results in induced apoptosis and programmed cell death or impairment of functions of said activated T cell.

Abstract: A multi-transmembrane protein antigen includes a polypeptide corresponding to an extracellular loop of the multi-transmembrane protein, the N-terminal and C-terminal of the polypeptide being fixed on a solid substrate or the N-terminal and C-terminal being attached to both ends of a linker to form a cyclic structure, an antibody specifically binding to the antigen or an antigen-binding fragment thereof, and a method for screening an antibody specifically binding to the antigen. The present invention may be usefully employed for effective production of antibodies for multi-transmembrane proteins that play important roles in disease-related phenomena such as cell signaling.

Abstract: Pre-implantation factor (PIF) may be used to treat intracellular damage. Aspects of the invention are directed to a method of treating intracellular damage comprising administering PIF to a subject in need thereof. Some aspects may be directed to methods of increasing cytokine secretion in response to intracellular damage comprising administering PIF to a subject in need thereof. The intracellular damage may be a result of a disease such as Listeria monocytogenes infection, malaria, Lyme disease, cardiovascular disease, duodenal peptic ulcer, atherosclerosis, peritonitis or tuberculosis. In some aspects, a method of treating tuberculosis is disclosed, comprising administering PIF to a subject in need thereof. In some aspects, a method of treating atherosclerosis is disclosed, comprising administering PIF to a subject in need thereof. In some aspects, a method of treating peritonitis is disclosed, comprising administering PIF to a subject in need thereof.

Abstract: The present invention relates to a fusion protein, comprising a cytokine antagonist and a targeting moiety, preferably an antibody or anti-body like molecule. In a preferred embodiment, the cytokine antagonist is a modified cytokine which binds to the receptor, but doesn't induce the receptor signalling. The invention relates further to a fusion protein according to the invention for use in treatment of cancer and immune- or inflammation-related disorders.

Abstract: The present invention provides a method for reducing the weight of a subject, preventing weight gain in a subject, lowering blood glucose, or treating hepatic steatosis, comprising administering to a subject in need thereof a therapeutically effective amount of a pharmaceutical composition comprising interleukin-25 or IL-25-activated macrophages. In addition, the present invention provides a method of treating cachexia or promoting weight gain in a mammal in need of such treatment, comprising administering to the mammal a therapeutically effective amount of a pharmaceutical composition comprising an inhibitor or antagonist of interleukin-25 in a mammal in the treatment of cachexia.

Abstract: The present invention relates to a novel epitope of IP-10 (IFN-?-inducible protein 10), to an antibody to the epitope or an antigen-binding fragment thereof, to a composition comprising the epitope as an active ingredient for inducing an antibody to IP-10, and to a pharmaceutical composition comprising the antibody or the antigen-binding fragment thereof for preventing or treating diseases relating to IP-10. The anti-IP-10 antibody of the present invention can be effectively used in preventing or treating various diseases relating to IP-10 such as multiple sclerosis, rheumatoid arthritis and systemic lupus erythematosus.