Abstract: The response of immunotherapy in the treatment of cancer is enhanced by use of an oligonucleotide in a dose effective to induce at least one of endogenous production of cytokines, and the regulation of the expression of one or more of the cell surface antigens (FIG. 1).

Abstract: Antibodies and antigen-binding fragments of antibodies that bind human CXCR3 are disclosed. In preferred embodiments, the antibodies are human. Nucleic acids and vectors encoding the antibodies or portions thereof, recombinant cells that contain the nucleic acids, and compositions comprising the antibodies or antigen-binding fragments are also disclosed. The invention also provides therapeutic and diagnostic methods which employ the antibodies and antigen-binding fragments.

Abstract: Pharmaceutical composition comprising an antibody specifically recognizing CD38 and melphalan.

Abstract: Immunostimulatory compositions and methods comprising an ITIM motif-containing DC immunoreceptor (DCIR) to mediate potent crosspresentation are described herein. The inventors evaluated human CD8+ T cell responses generated by targeting antigens to dendritic cells (DCs) through various lectin receptors. A single exposure to a low dose of anti-DCIR-antigen conjugate initiated antigen-specific CD8+ T cell immunity by all human DC subsets including ex vivo generated DCs, skin-isolated Langerhans cells and blood mDCs and pDCs. Enhanced specific CD8+ T cell responses were observed when antigens like, FluMP, MART-1, viral (HIV gag), etc. were delivered to the DCs via DCIR, compared to those induced by a free antigen, or antigen conjugated to a control mAb or delivered via DC-SIGN, another lectin receptor. Addition of Toll-like receptor (TLR) 7/8-agonist enhanced DCIR-mediated crosspresentation as well as crosspriming.

Abstract: The present invention relates generally to the use of bendamustine in combination with an anti-CD20 antibody to treat cancer.

Abstract: A method for treating psoriatic arthritis comprising an interleukin-6 (IL-6) antagonist such as, for example, an antibody against IL-6 receptor.

Abstract: Disclosed herein, in certain embodiments, is a method for treating an MIF-mediated disorder. In some embodiments, the method comprises administering an active agent that inhibits (i) MIF binding to CXCR2 and CXCR4 and/or (ii) MIF-activation of CXCR2 and CXCR4; (iii) the ability of MIF to form a homomultimer; or a combination thereof.

Abstract: The invention provides binding molecules, including antibody molecules which selectively bind to a cell surface antigen of a target cell, and wherein the binding molecules, on binding the cell surface antigen, induce apoptosis of the target cell. There is also provided methods of and pharmaceutical compositions for apoptosis induction and uses thereof.

Abstract: The present invention provides single nucleotide polymorphisms (SNPs) associated with clinical responsiveness of rheumatoid arthritis patients to treatment with an interleukin-6 receptor antibody such as tocilizumab, and methods of using such SNPs for predicting clinical response to treatment with the antibody.

Abstract: The present invention provides methods of detecting cancer using biomarkers.

Abstract: The present invention relates to methods for identifying and using modulators of FDF03 biological activity in vitro and in vivo that are useful in the treatment of cancer.

Abstract: Novel anti-cancer agents, including, but not limited to, antibodies and immunoconjugates, that bind to CD37 are provided. Methods of using the agents, antibodies, or immunoconjugates, such as methods of inhibiting tumor growth are further provided.

Abstract: A non-ordered geometric mesoporous structure that provides for enhanced loading of antibodies such as IgG as compared to ordered mesoporous structures. This structure is formed by treating silica precursors at a hydrothermal aging temperature between 100 and 200 degrees C. This creates the non-ordered mesoporous structure. Biomolecules such as IgG can then be spontaneously loaded via non-covalent bonding within the as-made or functionalized mesoporous structure.

Abstract: The present invention relates to a combined preparation comprising at least one rocaglamide derivative and at least one apoptosis inducing agent, preferably from the group of substances comprising agents inducing the extrinsic apoptotic pathway, antiproliferative agents and agents which induce apoptosis in T-cells by activation induced cell death (AICD) for the treatment of cancer.

Abstract: The present invention relates to the field of compositions comprising anti-CD5 antibodies. In particular, the present invention concerns an antibody composition comprising at least two anti-CD5 antibodies capable of binding distinct CD5 epitopes. The invention further concerns bi-specific molecules having the binding specificities of said antibody compositions. The invention also relates topharmaceutical compositions, use of antibody compositions and methods for manufacturing antibody compositions. The invention further relates to cell banks and a method for killing cells.

Abstract: This invention relates to compositions and methods comprising “lymphotoxin-?-receptor blocking agents”, which block lymphotoxin-? receptor signalling. Lymphotoxin-? receptor blocking agents are useful for treating lymphocyte-mediated immunological diseases, and more particularly, for inhibiting Th1 cell-mediated immune responses. This invention relates to soluble forms of the lymphotoxin-? receptor extracellular domain that act as lymphotoxin-? receptor blocking agents. This invention also relates to the use of antibodies directed against either the lymphotoxin-? receptor or its ligand, surface lymphotoxin, that act as lymphotoxin-? receptor blocking agents. A novel screening method for selecting soluble receptors, antibodies and other agents that block LT-? receptor signalling is provided.

Abstract: The present application is directed to the combination therapy of a type I and a type II anti-CD20 antibody for the treatment of cancer, especially of CD20 expressing cancer.

Abstract: Disclosed herein are methods and compositions comprising anti-CD74 and/or anti-HLA-DR antibodies for treatment of GVHD and other immune dysfunction diseases. In preferred embodiments, the anti-CD74 and/or anti-HLA-DR antibodies are effective to deplete antigen-presenting cells, such as dendritic cells. Most preferably, administration of the therapeutic compositions depletes all subsets of APCs, including mDCs, pDCs, B cells and monocytes, without significant depletion of T cells. In alternative embodiments, administration of the therapeutic compositions suppresses proliferation of allo-reactive T cells, while preserving cytomegalovirus (CMV)-specific, CD8+ memory T cells. The compositions and methods provide a novel conditioning regimen for preventing aGVHD and/or treating chronic GVHD, without altering preexisting anti-viral immunity.

Abstract: The efficacy of light activated therapy treatment is enhanced by stimulating the immune system of the patient substantially above a normal level. Abnormal tissue that is destroyed by the light activated therapy releases factors that stimulate the immune system, leading to systemic reductions in abnormal tissue (i.e., reduction beyond the region treated using light). By further stimulating the immune system using an anti-CTLA-4 antibody, the systemic destruction of abnormal tissue is enhanced.

Abstract: The invention describes methods for inhibiting angiogenesis in a tissue by administering an antagonist that specifically binds to a proteolyzed or denatured collagen but not to native triple helical forms of the collagen. Antagonists of the invention can target, for example, denatured collagens type-I, type-II, type-III, type-IV, type-V and combinations thereof. Methods utilizing such antagonists for therapeutic treatment of tumor growth, tumor metastasis or of restenosis also are described, as are methods to use such antagonists as diagnostic markers of angiogenesis is normal or diseased tissues both in vivo and ex vivo. Antagonists include monoclonal antibodies referred to as HUI77, HUIV26, and XL313.

Abstract: The present invention provides a new method for the prediction of, or diagnosis of, auto-immune diseases, thereby alerting the subject to the presence of, or propensity to develop, an auto-immune disease so that preventative or therapeutic regiments may be initiated or changed so as to treat, modulate or prevent expansion of the CD4loCD40hi T cell population responsible for the destructive inflammation. The invention also discloses agents which modulate, treat or prevent expansion of CD4loCD40hi T cells. In one embodiment, the method is predictive of type 1 diabetes.

Abstract: The present invention provides a method of inhibiting survival of T helper 1 (Th1) memory cells by contacting or administering a population of Th1 cells with an agent that inhibits CD44 receptor expression or activation. The invention further provides a method of stimulating memory Th1 cell survival comprising contacting or administering Th1 cells with an agent that increases CD44 receptor activation or expression in the cells. The invention additionally provides a method of screening for agents capable of modulating Th1 cell survival.

Abstract: This invention relates to compositions and methods for treating c-Kit associated disorders such as fibrosis, and more particularly, to compositions containing humanized c-Kit antibodies.

Abstract: The invention provides antibody to canine or feline or equine antigens. Specifically, antibodies directed to canine CD20 which have been caninized or felinized are provided. Also provided are methods for preparing high affinity antibodies to canine and feline CD20 as well as methods for treating B cell disorders in companion animals.

Abstract: The disclosure provides, inter alia, binding proteins (e.g., antibodies) that bind to an integrin in an activated conformation, e.g., activated LFA-1 (“aLFA-1”), e.g., relative to a non-activated conformation of LFA-1. In one embodiment, the binding proteins inhibit at least one function of an aLFA-1, e.g., inhibit a binding interaction between aLFA-1 and a cognate ligand of aLFA-1, e.g., an ICAM protein. The binding proteins can be used to treat or prevent an inflammatory disorder or other disorder.

Abstract: Compositions and methods are provided for screening and identifying compounds which modulate signaling of toll-like receptor 4 (TLR4) pathway via CD 14 and a ligand. Methods are provided for treatment of various disease states such as inflammation or autoimmune disease in mammalian subjects by modulating toll-like receptor 4 (TLR4) pathway signaling via CD 14 and a ligand. Transgenic non-human animals and methods for developing transgenic non-human animals are provided wherein the transgenic non-human animals comprise a loss-of-function mutation in the CD 14 gene.

Abstract: Biomarkers associated with inflammatory bowel disease (IBD) are provided, as well as methods of using such biomarkers for diagnosing, assessing and monitoring disease progression. The biomarkers may be measured at the protein level or the gene expression level Biomarkers may be tracked individually or in groups of two or more. The disclosed biomarkers may find particular utility in monitoring a course of therapy, such as treatment with an IL-23 antagonist. Changes in biomarker levels can also be used to confirm target engagement and therapeutic efficacy. Changes in biomarkers can also be used inform modification of a therapeutic regimen, for example to increase or decrease dosing of a therapeutic agent, such as an anti-IL-23 or anti-IL-23R anti-body.

Abstract: The present disclosure relates to a composition for targeting dendritic cells. In particular, the present disclosure relates to a composition comprising: a) one or more antigens; b) an anti-DC-SIGN immunoglobulin single variable domain; and c) a carrier which carries a) and b). The disclosure further relates to formulations, compositions and devices comprising such anti-DC-SIGN molecules and their use as a medicament and in the treatment of cancer, suitably melanoma.

Abstract: Provided are methods and compositions for treating and/or preventing an autoimmune diseases, including inflammatory bowel disease, rheumatoid arthritis, diabetes mellitus, celiac disease, autoimmune thyroid disease, autoimmune liver disease, Addison's Disease, Sjögren's Syndrome, transplant rejection, graft vs. host disease, or host vs. graft disease.

Abstract: A therapeutic agent for chronic arthritides diseases of childhood-related diseases, for example chronic arthritides diseases of childhood, Still's disease and the like, comprising an interleukin-6 (IL-6) antagonist as an active ingredient.

Abstract: Uses of anti-CS1 antibodies, alone or in combination with other agents, for the treatment of rare lymphomas, such as NK lymphomas, NK/T-cell lymphomas, and angioimmunoblastic lymphomas.

Abstract: The present invention relates to antibodies that bind CD33. More particularly, the invention relates to anti-CD33 antibodies, fragments and homologues of these antibodies, humanized and resurfaced versions of these antibodies, functional equivalents and improved versions of these antibodies, immunoconjugates and compositions comprising these antibodies, and the uses of same in diagnostic, research and therapeutic applications. The invention also relates to a polynucleotide encoding these antibodies, vectors comprising the polynucleotides, host cells transformed with polynucleotides and methods of producing these antibodies.

Abstract: A synergistic adjuvant is provided comprising synergistically effective amounts of at least one type 1 interferon and at least one CD40 agonist, wherein these moieties may be in the same or separate compositions. In addition, fusion proteins and DNA conjugates which contain a type 1 interferon/CD40 agonist/antigen combination are provided. The use of these compositions, protein and DNA conjugates as immune adjuvants for treatment of various chronic diseases such as HIV infection and for enhancing the efficacy of vaccines (prophylactic and therapeutic) is also provided.

Abstract: Host nucleic acids and host proteins that participate in viral infection, such as human immunodeficiency virus (HIV), influenza A, and Ebola virus, have been identified. Interfering with or disrupting the interaction between a host nucleic acid or host protein and a virus or viral protein confers an inhibition of or resistance to infection. Thus, interfering with such an interaction in a host subject can confer a therapeutic or prophylactic effect against a virus. The sequences identified can be used to identify agents that reduce or inhibit viral infection.

Abstract: Methods of treating hemorheologic abnormalities in mammals are provided, as well as methods of evaluating circulatory flow mechanics by analyzing hemorheologic determinants or hemorheologic abnormalities in the blood.

Abstract: A method of diagnosing B-CLL in a subject in need thereof is provided. The method comprising determining in a biological sample of the subject a level of CD84 isoform C (SEQ ID NO: 30), wherein an increase in the level of the CD84 isoform C (SEQ ID NO: 30) beyond a predetermined threshold with respect to a level of the CD84 in a biological sample from a healthy individual is indicative of the B-CLL.

Abstract: The present invention relates to methods for modulating a ?-cell population using a TM4SF4 modulator or a modulator of a TM4SF4 homolog. More particularly, the invention relates, inter alia, to methods and compositions for generating, expanding, and maintaining a ?-cell population and treatment of diseases associated with the loss of ?-cells using a TM4SF4 modulator or a modulator of a TM4SF4 homolog.

Abstract: The invention relates to methods for treating and diagnosing hematologic malignancies, Chronic lymphocytic leukemia and Small Lymphocytic Lymphoma in particular, using PD-1 ligands (PD-L1, PD-L2 or anti-PD-1 antibodies).

Abstract: A novel polypeptide ligand, p30, or LIGHT, for herpes virus entry mediator, HVEM, is provided. LIGHT is useful for modulating immune responses and in inhibiting infection and/or subsequent proliferation by herpesvirus. HVEM fusion proteins are also provided. Methods for treating subjects with lymphoid cell disorders, tumors, autoimmune diseases, inflammatory disorders or those having or suspected of having a herpesvirus infection, utilizing p30 and the fusion proteins of the invention, are also provided.

Abstract: The invention provides a tumor cell genetically modified to express a nucleic acid encoding a secreted form of a heat shock protein (hsp) gp96 polypeptide. The invention also provides a method of stimulating an immune response to a tumor by administering a tumor cell genetically modified to express a nucleic acid encoding a secreted form of a gp96 polypeptide.

Abstract: The invention relates to the use of a binding member which binds to LewisY and Lewisb haptens in the treatment of tumours and leukaemia. The binding member may be an antibody which binds to LewisY and Lewisb haptens and cancer cells and induces cells death.

Abstract: The present invention relates to a phenotypically distinct CD1dhigh CD5+ B cell subset that regulates T cell mediated inflammatory responses through the secretion of interleukin-10 (IL-IO). The invention also relates to the use of these IL-IO producing regulatory B cells in the manipulation of immune and inflammatory responses, and in the treatment of disease. Therapeutic approaches involving adoptive transfer of these regulatory B cells, or expansion of their endogenous levels for controlling autoimmune or inflammatory diseases and conditions are described. Ablation of this subset of regulatory B cells, or inhibition of their IL-IO production can be used to upregulate immunodeficient conditions, and/or to treat tumors/cancer. Diagnostic applications also are encompassed.

Abstract: The present invention relates to nucleic acid molecules encoding Neutrokine-alpha and/or Neutrokine-alphaSV polypeptides, including soluble forms of the extracellular domain. Neutrokine-alpha and/or Neutrokine-alphaSV polypeptides are also provided as are vectors, host cells and recombinant methods for producing the same. The invention further relates to antibodies or portions thereof that specifically bind Neutrokine-alpha and/or Neutrokine-alphaSV and diagnostic and therapeutic methods using these antibodies. Also provided are diagnostic methods for detecting immune system-related disorders and therapeutic methods for treating immune system-related disorders using the compositions of the invention.

Abstract: Antibodies directed to the antigen CD20 and uses of such antibodies are disclosed herein. In particular, fully human monoclonal antibodies directed to the antigen CD20. Nucleotide sequences encoding, and amino acid sequences comprising, heavy and light chain immunoglobulin molecules, particularly sequences corresponding to contiguous heavy and light chain sequences spanning the framework regions and/or complementarity determining regions (CDR's), specifically from FR1 through FR4 or CDR1 through CDR3 are disclosed. Hybridomas or other cell lines expressing such immunoglobulin molecules and monoclonal antibodies are also disclosed.

Abstract: The present invention provides binding molecules, such as human binding molecules, that bind to and stimulate the human OX40-receptor. The invention also provides nucleic acids encoding such binding molecules. Methods for producing such binding molecules are also provided by the present invention. The binding molecules and nucleic acids are useful in the stimulation of human T-cells and can be used to enhance antigen-specific immune responses.

Abstract: The present invention relates to therapeutic targets for multiple sclerosis and other inflammatory and neurological diseases. In particular, the present invention relates to altering G-CSF/G-CSFR signaling in the treatment of such disorders.

Abstract: Provided are methods and compositions for detecting and treating normal, hypoplastic, ectopic or remnant tissue, organ or cells in a mammal. The method comprises parenterally injecting a mammalian subject, at a locus and by a route providing access to said tissue or organ, with an composition comprising antibody/fragment which specifically binds to targeted organ, tissue or cell. The antibody/fragment may be administered alone, or labeled or conjugated with an imaging, therapeutic, cytoprotective or activating agent.

Abstract: The invention relates to immunoglobulin single variable domains directed against specific human CXCR4 epitopes (herein also referred to interchangeably as “compounds of the invention”, “amino acid sequences of the invention”, or “building blocks of the invention”) and polypeptides comprising them (herein also referred to as “polypeptides of the invention”, “compounds of the invention”, or “constructs of the invention”).

Abstract: Biomarkers for predicting the severity of malaria and methods for their detection are disclosed. In one aspect, the present application discloses CXCL4, CXCL10, VEGF, PGDF, IL-1Ra, IL-8, MIP-1?, sFas, Fas-L, sTNF-R2, and sTNF-R1 as biomarkers for the severity of malaria. In another aspect, the present application discloses a method for determining the severity of malaria and predicting mortality due to cerebral malaria. The method comprises the detection of the biomarkers CXCL4 and/or CXCL10 and at least one more biomarker and determining the severity of malaria and predicting mortality due to cerebral malaria based upon the ratio of expression of the biomarkers in the subject versus the expression of the biomarkers in a control.

Abstract: The present invention relates to a composition for eliciting a specific cytotoxic T lymphocyte (CTL) response against T cell epitopes in a mammal, which comprises a compound provoking lymphocytopenia, a molecule having selective affinity for professional antigen presenting cells (APC), wherein said molecule is associated to said T cell epitope, and optionally, a pharmaceutical acceptable carrier. Advantageously, the composition further contains an adjuvant. Said composition may be used in anti-infections and anti-cancer therapies.