Abstract: Disclosed are compositions and methods for stimulating immune responses. More particularly, these compositions and methods involve the use of an inhibitor of IL-25 function and an immune stimulator that stimulates an immune response to a target antigen for stimulating protective or therapeutic immune responses to a target antigen. The compositions and methods of the present invention are particularly useful in the prevention and treatment of infections and cancers.

Abstract: The present invention is based on the seminal discovery that targeted immunomodulatory antibodies and fusion proteins can counter act or reverse immune tolerance of cancer cells. Cancer cells are able to escape elimination by chemotherapeutic agents or tumor-targeted antibodies via specific immunosuppressive mechanisms in the tumor microenvironment and such ability of cancer cells is recognized as immune tolerance. Such immunosuppressive mechanisms include immunosuppressive cytokines (for example, Transforming growth factor beta (TGF-?)) and regulatory T cells and/or immunosuppressive myeloid dendritic cells (DCs). By counteracting tumor-induced immune tolerance, the present invention provides effective compositions and methods for cancer treatment, optional in combination with another existing cancer treatment.

Abstract: Nucleic acid molecules and compositions comprising: a nucleic acid sequence that encodes IL-12 p35 subunit or a functional fragment thereof and/or a nucleic acid sequence that encodes IL12 p40 subunit or a functional fragment thereof, are disclosed. The nucleic acid molecules and compositions further comprising a nucleic acid sequence that encodes an immunogen are also disclosed. Method of modulating immune response and methods of inducing an immune response against an immunogen are disclosed. Therapeutic and prophylactic vaccination methods are also disclosed.

Abstract: Disclosed herein are methods for selectively treating pruritus in a subject having chronic prurigo (CP), including prurigo nodularis (PN), pharmaceutical compositions for use in the treatment of pruritus in a subject having CP or PN, uses of nemolizumab or an equivalent thereof in the manufacture of a medicament for the treatment of pruritus in a subject having CP or PN.

Abstract: The present invention relates to the use of the Chemokine (C—C motif) ligand 20 (CCL20) as a biomarker to stratify or identify populations of patients suffering from interleukin-23 (IL23)-mediated diseases (e.g., Crohn's disease) responsive to treatment with an, anti-IL23 antagonist (including, e.g., anti-IL23 antibodies). Levels of CCL20 above or below a predetermined threshold can be used, for example, (i) to determine whether a patient with an IL23-mediated disease or disorder such a Crohn's disease is eligible or non-eligible for treatment with a therapeutic agent, (ii) to determine whether treatment with a certain agent should be commenced, suspended, or modified, (iii) to diagnose whether the IL23-mediated disease is treatable or not treatable with a specific therapeutic agent, or (iv) to predict the outcome of treating the IL23-mediated disease with a specific therapeutic agent. CCL20 can be used in combination with other IL23 pathway biomarkers such as IL22 and/or lipocalin-2 (LCN2).

Abstract: The present invention provides methods for decreasing a nasal polyp score in a subject. The methods include administering to a subject in need thereof a therapeutic composition comprising an interleukin-4 receptor (IL-4R) antagonist such as an anti-IL-4R antibody or antigen binding fragment thereof.

Abstract: The invention features multi-specific protein complexes with one domain comprising IL-15 or a functional variant and a binding domain specific to a disease antigen, immune checkpoint or signaling molecule.

Abstract: A method of treating an IL-12/23-related disease in a patient using an increasing dosing interval, comprises increasing the dosing interval of IL-12/IL-23 antibody to a patient, wherein the antibody is administered initially and after 4 weeks, after 16 weeks and after 28 weeks, and increasing the dosing interval after 28 weeks to an increased interval, e.g., every 16, 20 or 24 weeks.

Abstract: The disclosure provides, inter alia, methods of detecting IL-6 signaling activity in T cells in breast cancer patients, such as breast cancer patients in remission.

Abstract: The invention features combination therapies using an IL-15-based superagonist complex and an antibody to effectively treat subjects with cancer and infectious diseases.

Abstract: The present invention provides methods for treating moderate-to-severe or severe atopic dermatitis (AD). The methods of the present invention comprise administering to a subject in need thereof one or more doses of an interleukin-4 receptor (IL-4R) inhibitor such as an anti-IL-4R antibody. In certain embodiments, the methods of the present invention are used to treat severe AD in a patient whose disease is not controlled with systemic therapy (e.g., cyclosporine A) or when such therapy is inadvisable.

Abstract: The invention features multi-specific protein complexes with one domain comprising IL-15 or a functional variant, a cytokine receptor or cytokine ligand, and a binding domain specific to a disease antigen, immune checkpoint or signaling molecule.

Abstract: The disclosure provides antibody agents that bind to a programmed death-1 (PD-1) protein. Particular immunoglobulin heavy chain polypeptide and immunoglobulin light chain polypeptide sequences are explicitly provided. Also provided are related nucleic acids, vectors, compositions, and methods of using the anti-PD-1 antibody agent to treat a disorder or disease that is responsive to PD-1 inhibition, such as cancer or an infectious disease.

Abstract: The present disclosure provides methods of evaluating a subject, e.g., a subject at risk for or suffering from a pKal-mediated or bradykinin-mediated disorder, based on values (e.g., percentages) of intact and/or cleaved kininogen in a sample of the subject. Provided methods permit analysis of patients with plasma kallikrein-mediated angioedema (KMA), or other diseases mediated by pKal useful in the evaluation and treatment. Such methods can involve the use of a detection agent that preferentially binds cleaved kininogen or intact kininogen.

Abstract: The present invention discloses IL-13 antibody, method of its preparation and use thereof. The IL-13 antibody comprises one or more of heavy chain CDR1, heavy chain CDR2 and heavy chain CDR3 of heavy chain variable region of the IL-13 antibody, and/or one or more of light chain CDR1, light chain CDR2, and light chain CDR3 of light chain variable region of the IL-13 antibody. The IL-13 antibody has a high affinity and can significantly inhibit the secretion of thymus activation-regulated chemokine and periostin as well as the expression of vascular cell adhesion molecule-1 induced by IL-13, it can significantly inhibit airway hyperresponsiveness in mice induced by IL-13, and therefore can be used in the preparation of drugs for preventing or treating IL-13 expression or dysfunction related diseases.

Abstract: The present invention generally relates to antigen-specific immunoconjugates for selectively delivering effector moieties that influence cellular activity. More specifically, the invention provides novel immunoconjugates comprising a first antigen binding moiety, an Fc domain and a single effector moiety. In addition, the present invention relates to polynucleotides encoding such immunoconjugates, and vectors and host cells comprising such polynucleotides. The invention further relates to methods for producing the immunoconjugates of the invention, and to methods of using these immunoconjugates in the treatment of disease.

Abstract: Provided herein are activatable anti-human CTLA-4 antibodies comprising a heavy chain comprising a VH domain and a light chain comprising a masking moiety (MM), a cleavable moiety (CM), and a VL domain. Such activatable anti-human CTLA-4 antibodies have CTLA-4 binding activity in the tumor microenvironment, where the masking moiety is removed by proteolytic cleavage of the cleavable moiety by tumor-specific proteases, but exhibit greatly reduced binding to CTLA-4 outside the tumor. In this way, the activatable anti-human CTLA-4 antibodies of the present invention retain anti-tumor activity while reducing the side effects associated with anti-CTLA-4 activity outside the tumor.

Abstract: Antibodies and antigen binding fragments that specifically bind to IL-7R? are disclosed. Nucleic acids encoding the antibodies and antigen binding fragments, and vectors including the nucleic acid molecules are also provided. Methods for detecting a ca cancer or a cell that expresses IL-7R? using the antibodies and antigen binding fragments are disclosed, as is the use of the antibodies and antigen binding fragments to prevent and/or treat a subject with a cancer that expresses IL-7R?, such as acute lymphoblastic leukemia.

Abstract: The present invention concerns antigen binding proteins that bind TL1A, including bispecific antigen binding proteins (e.g., antibodies) to TL1A and TNF-?. Such bispecific antibodies can be in a tetrameric immunoglobulin format, in which one heavy chain-light chain pair of the antibody is directed to TL1A and the other to TNF-?. The bispecific antigen binding proteins may also be comprised in an IgG-scFv fusion, in which a conventional tetrameric antibody directed to one antigen is fused to a pair of single chain Fv units directed to the other. The bispecific antigen binding protein may also be comprised in an IgG-Fab fusion, in which a Fab molecule that binds to one antigen is fused to each heavy chain of a conventional tetrameric antibody directed to the other antigen. The invention further relates to uses of the anti-TL1A binding proteins and anti-TL1A/anti-TNF-? antigen binding proteins, and pharmaceutical formulations thereof.

Abstract: The present invention is directed to a novel targeted heterodimeric Fc fusion proteins comprising an IL-15/IL-15R? Fc fusion protein and an antigen binding domain Fc fusion proteins. In some instances, the antigen binding domain binds to CD8, NKG2A, or NKG2D.