Abstract: The invention provides peptides and fragments, methods and uses based upon modulating the binding or interaction between 4-1BB and galectins such as Galectin-9. Modulating such binding or interaction between 4-1BB and a galectin, such as Galectin 9. modulates an immune response.

Abstract: The invention relates to compositions, methods and uses of inhibitors of binding between PKC? and CD28, and modulating an undesirable or aberrant immune response, disorder or disease, an inflammatory response, disorder or disease, inflammation or an autoimmune response, disorder or disease. Compositions include inhibitors of binding between PKC? and CD28, which include, among others, PKC?, CD28 and Lck sequences, subsequences, variants and modified forms, and polymorphisms.

Abstract: The invention relates to antibodies and subsequences thereof that specifically bind to poxvirus B5R envelope protein, antibodies and subsequences thereof that specifically bind to poxvirus H3L envelope protein, and combinations thereof.

Abstract: A composition comprising a TRAIL-R2 receptor or fragment thereof bound to a ligand in crystalline form is presently provided along with novel binding sites and binding agents of a TRAIL receptor. Also provided are methods of designing a compound, protein or peptide and identifying a binding agent that interacts with a TRAIL receptor. The present invention further provides methods of modulating binding of a TRAIL receptor to a ligand, the methods comprising contacting the TRAIL receptor with a binding agent, ligand, or an agonist or antagonist thereof, that interacts with a novel binding site described herein.

Abstract: The invention provides antibodies that specifically bind to OX40 (CD134), referred to as OX40 antibodies, anti-OX40 or anti-OX40 antibodies. Invention antibodies that specifically bind to OX40 include mammalian (human, primate, etc.), humanized and chimeric anti-OX40 antibodies. Invention antibodies and antibody subsequences (fragments) that specifically bind to OX40 include purified and isolated antibodies, as well as pharmaceutical formulations thereof, are useful in various methods including treatment, screening and detection methods.

Abstract: The invention relates to antibodies and subsequences thereof that specifically bind to poxvirus B5R envelope protein, antibodies and subsequences thereof that specifically bind to pox virus H3L envelope protein, and combinations thereof.

Abstract: The present invention relates to M. tuberculosis proteins and peptides, and subsequences, portions or modifications thereof and methods and compounds comprising the same for eliciting, stimulating, inducing, promoting, increasing, or enhancing an anti-M. tuberculosis immune response in a subject.

Abstract: T cell memory can persist in the absence of antigen. However, some memory cells by default are subject to signals accompanying periodic antigen exposure. OX40 is essential to the extent and persistence of Th2 memory when antigen is re-encountered. In an animal model of allergic asthma, inhibiting OX40/OX40L signaling during the secondary response to inhaled antigen suppressed lung inflammation. Inhibiting OX40 at the time of memory cell reactivation reduced the longevity of memory with further inflammation prevented upon tertiary encounter with antigen.

Abstract: Provided herein are antibodies that immunospecifically bind to an hLIGHT polypeptide; isolated nucleic acids encoding the antibodies; vectors and host cells comprising nucleic acids encoding the antibodies; methods of making the antibodies; and a method of treating a hLIGHT-mediated disease in a subject comprising administering to the subject the antibodies. In preferred embodiments, the anti-hLIGHT antibodies provided herein will ameliorate, neutralize or otherwise inhibit hLIGHT biological activity in vivo (e.g., the hLIGHT-mediated production or secretion of CCL20, IL-8 or RANTES from a cell expressing a hLIGHT receptor). Also provided herein is a method for the detection of hLIGHT in a sample as well as a method for ameliorating, neutralizing or otherwise inhibiting hLIGHT activity, e.g., in a human subject suffering from a disorder in which hLIGHT activity is detrimental.

Abstract: Dengue virus (DV) peptides, including T cell epitopes, structural and non-structural (NS) polypeptide sequences, subsequences and modifications thereof, nucleotide sequences encoding such peptides, and compositions including such peptides and encoding nucleotide sequences, and cells expressing such peptides, are provided. Such DV peptides, nucleotide sequences and compositions, can be used to elicit, stimulate, induce, promote, increase, enhance or activate an anti-DV CD8+ T cell response or an anti-DV CD4+ T cell response. Such peptides, nucleotide sequences and compositions can also be used for and in methods of vaccination/immunization of a subject against Dengue virus (DV) (e.g., to provide protection against DV infection and/or pathology), and for treatment of a subject in need thereof, for example, treatment of the subject for a Dengue virus (DV) infection or pathology.

Abstract: Provided herein, inter alia, are compositions and methods of measuring levels of RPTP protein and RNA and treating subjects with certain diseases, such as autimmune diseases.

Abstract: Provided herein are antibodies that immunospecifically bind to an hLIGHT polypeptide; isolated nucleic acids encoding the antibodies; vectors and host cells comprising nucleic acids encoding the antibodies; methods of making the antibodies; and a method of treating a hLIGHT-mediated disease in a subject comprising administering to the subject the antibodies. In preferred embodiments, the anti-hLIGHT antibodies provided herein will ameliorate, neutralize or otherwise inhibit hLIGHT biological activity in vivo (e.g., the hLIGHT-mediated production or secretion of CCL20, IL-8 or RANTES from a cell expressing a hLIGHT receptor). Also provided herein is a method for the detection of hLIGHT in a sample as well as a method for ameliorating, neutralizing or otherwise inhibiting hLIGHT activity, e.g., in a human subject suffering from a disorder in which hLIGHT activity is detrimental.

Abstract: Methods of decreasing, reducing, inhibiting, suppressing, limiting or controlling an undesirable or aberrant immune response, immune disorder, inflammatory response, or inflammation in a subject; decreasing, reducing, inhibiting, suppressing, limiting or controlling an autoimmune response, disorder or disease in a subject; and decreasing, reducing, inhibiting, suppressing, limiting or controlling an adverse cardiovascular event or cardiovascular disease in a subject, are provided. Methods include, for example, administering a Nur77 polypeptide or subsequence thereof, a Nur77 agonist, or CD14+ CD16+ monocytes or CD14dimCD16+ (CD115+CD11b+GR1? (Ly6C?)) monocytes or macrophages to a subject to decrease, reduce, inhibit, suppress, limit or control the underlying condition or an adverse symptom or pathology of the condition.

Abstract: The invention provides Galectin-3 binding protein (Gal-3BP, BTBD17B) polypeptides, Gal-3BP compositions, and methods of use, and uses, for example, in treatment, diagnostic, detection and prognostic methods, such as treatment of an undesirable or aberrant immune response, immune disorder, inflammatory response, or inflammation, and treatment of an autoimmune response, disorder or disease.

Abstract: Methods of treating a food allergy, allergic reactions, hypersensitivity, inflammatory responses, inflammation are provided. In one method, histamine releasing factor (HRF)/translationally controlled tumor protein (TCTP) is contacted with a compound that inhibits or reduces binding of HRF/TCTP to an immunoglobulin in order to treat the food allergy, allergic reaction, hypersensitivity, inflammatory response, or inflammation. Methods of reducing or decreasing the probability, severity, frequency, duration or preventing a subject from having an acute or chronic food allergy, allergic reaction, hypersensitivity, an inflammatory response or inflammation, are also provided.

Abstract: Herpesvirus entry mediator (HVEM) is a member of the tumor necrosis factor receptor superfamily (TNFRSF) and acts as a molecular switch that modulates T cell activation by propagating positive signals from the TNF related ligand, LIGHT (p30, TNFSF14), or inhibitory signals through the immunoglobulin superfamily member, B and T lymphocyte attenuator (BTLA). A novel binding site for BTLA is disclosed, located in cysteine-rich domain-1 of HVEM. BTLA binding site on HVEM overlaps with the binding site for the Herpes Simplex virus-1 envelope glycoprotein D (gD), but is distinct from where LIGHT binds, yet gD inhibits the binding of both ligands. A BTLA activating protein present in human cytomegalovirus is identified as UL144. UL144 binds BTLA, but not LIGHT, and inhibits T cell proliferation.

Abstract: The invention provides antibodies that specifically bind to OX40 (CD134), referred to as OX40 antibodies, anti-OX40 or anti-OX40 antibodies. Invention antibodies that specifically bind to OX40 include mammalian (human, primate, etc.), humanized and chimeric anti-OX40 antibodies. Invention antibodies and antibody subsequences (fragments) that specifically bind to OX40 include purified and isolated antibodies, as well as pharmaceutical formulations thereof, are useful in various methods including treatment, screening and detection methods.

Abstract: The invention provides human lymphoid tissue inducer (LTi) cells, methods of producing human lymphoid tissue inducer (LTi) cells, and methods of using human lymphoid tissue inducer (LTi) cells. Such methods include treatment of a subject that would benefit from human lymphoid tissue inducer (LTi) cells, for example, an immunocompromised or immunosuppressed subject.

Abstract: The invention relates to compositions and methods that employ OX40 (CD134), a TNFR superfamily protein, agonists. The invention includes among other things administering an OX40 agonist alone or in combination with a viral antigen, or live or attenuated virus, to treat a viral infection, or for vaccination or immunization.

Abstract: The present invention provides methods for restoring and increasing dendritic cell populations in a subject by modulation of the lymphotoxin-? receptor (LT?R) via LT?R agonists. The invention also provides methods for screening for agents capable of restoring or increasing dendritic cell populations. The invention further provides a method for the treatment of immunodeficiency by administration of an LT?R agonist.