Abstract: This disclosure provides a robust, sensitive, and specific assay for the detection and measurement of periostin levels in samples obtained from human patients having, or suspected of having an IL-13-mediated disease or disorder. The disclosure further provides novel antiperiostin monoclonal antibodies that recognize at least isoforms 1, 2, 3, 4, 7, and 8 of human periostin, and assay kits comprising one or more of these antibodies.

Abstract: The disclosure provides methods for treating lung cancer (e.g., non-small cell lung cancer) with an anti-PD-L1 antibody in a patient identified using a polynucleotide or polypeptide marker of the disclosure: CXCL9, KRT8, TRIM29, and/or IFNgamma.

Abstract: The present invention encompasses type-I IFN and IFN?-induced PD marker expression profiles, kits, and methods for identifying such IFN?-induced PD marker expression profiles. The type-I IFN and IFN?-induced PD marker expression profiles may also be used in, for example, methods of treating patients having a type-I IFN or IFN?-mediated disorder, methods of monitoring disease progression of patients receiving treatment with a therapeutic agent that binds to and modulates IFN? activity, identifying patients as candidates to receive a therapeutic that binds to and neutralizes IFN? activity, and in diagnosing or providing a prognosis to patients having IFN?-induced disorders.

Abstract: The invention provides compositions and methods featuring the use of miR-629 for identifying subjects responsive to B-cell depleting therapies (e.g., treatment with an anti-CD19 antibody). In other embodiments, the invention features the use of miR-629 to identify subjects as having a B cell malignancy.

Abstract: 13 antagonist, (iv) to prognosticate the outcome of treating an IL-13 mediated condition or disorder with a specific IL-13 antagonist. The disclosure further provides assay kits for the detection of DPP4, as well as computer implemented diagnostic methods.

Abstract: The disclosure provides methods for treating a subject having a type I IFN-mediated disease or disorder comprising administration of a fixed does of an anti-interferon alpha receptor antibody. The disclosure also provides methods for suppressing a type I interferon (IFN) gene signature (GS) in a subject. In addition, the disclosure provides methods of prognosing or monitoring disease progression in a subject having a type I IFN-mediated disease or disorder, methods of predicting a dosage regimen, methods of identifying a candidate therapeutic agent, methods of identifying a patient as a candidate for a therapeutic agent, and methods of designating a personalized therapy.

Abstract: This disclosure provides a robust, sensitive, and specific assay for the detection and measurement of periostin levels in samples obtained from human patients having, or suspected of having an IL-13-mediated disease or disorder. The disclosure further provides novel antiperiostin monoclonal antibodies that recognize at least isoforms 1, 2, 3, 4, 7, and 8 of human periostin, and assay kits comprising one or more of these antibodies.

Abstract: The present disclosure encompasses type-I IFN and IFN?-induced PD marker expression profiles, kits, and methods for identifying such IFN?-induced PD marker expression profiles. The type-I IFN and IFN?-induced PD marker expression profiles may also be used in, for example, methods of treating patients having a type-I IFN or IFN?-mediated disorder, methods of monitoring disease progression of patients receiving treatment with a therapeutic agent that modulates type 1 interferon activity, identifying patients as candidates to receive a therapeutic that binds to and neutralizes IFN? activity, and in diagnosing or providing a prognosis to patients having IFN?-induced disorders.

Abstract: The present invention provides anti-human ICOS antibodies with increased effector function. The invention further relates to pharmaceutical compositions, immunotherapeutic compositions, and methods using therapeutic antibodies that bind to the human ICOS antigen and that may mediate ADCC, CDC, and/or antibody-dependent phagocytosis (opsonization) for the treatment and prevention of T cell-mediated diseases and disorders, such as, but not limited to, chronic infection, autoimmune disease or disorder, inflammatory disease or disorder, graft-versus-host disease (GVHD), transplant rejection, and T cell proliferative disorder.

Abstract: Without limitation, this disclosure relates to compositions and methods for detecting and quantifying the expression of insulin receptor isoform A (IR-A) and/or insulin receptor isoform B (IR-B) in a tissue sample. The disclosure also relates to methods of diagnosis and classification based at least in part upon detecting and quantifying the expression of insulin receptor isoform A (IR-A) and/or insulin B (IR-B) in a tissue sample. Methods of treating a subject based upon such a classification are among additional aspects of the disclosure presented herein.

Abstract: The invention provides compositions and methods featuring the use of miR-629 for identifying subjects responsive to B-cell depleting therapies (e.g., treatment with an anti-CD19 antibody). In other embodiments, the invention features the use of miR-629 to identify subjects as having a B cell malignancy.

Abstract: The present disclosure encompasses type-I IFN and IFN?-induced PD marker expression profiles, kits, and methods for identifying such IFN?-induced PD marker expression profiles. The type-I IFN and IFN?-induced PD marker expression profiles may also be used in, for example, methods of treating patients having a type-I IFN or IFN?-mediated disorder, methods of monitoring disease progression of patients receiving treatment with a therapeutic agent that modulates type 1 interferon activity, identifying patients as candidates to receive a therapeutic that binds to and neutralizes IFN? activity, and in diagnosing or providing a prognosis to patients having IFN?-induced disorders.

Abstract: The disclosure provides methods for treating a subject having a type I IFN-mediated disease or disorder comprising administration of a fixed does of an anti-interferon alpha receptor antibody. The disclosure also provides methods for suppressing a type I interferon (IFN) gene signature (GS) in a subject. In addition, the disclosure provides methods of prognosing or monitoring disease progression in a subject having a type I IFN-mediated disease or disorder, methods of predicting a dosage regimen, methods of identifying a candidate therapeutic agent, methods of identifying a patient as a candidate for a therapeutic agent, and methods of designating a personalized therapy.

Abstract: The present invention encompasses type-I IFN and IFN?-induced PD marker expression profiles, kits, and methods for identifying such IFN?-induced PD marker expression profiles. The type-I IFN and IFN?-induced PD marker expression profiles may also be used in, for example, methods of treating patients having a type-I IFN or IFN?-mediated disorder, methods of monitoring disease progression of patients receiving treatment with a therapeutic agent that binds to and modulates IFN? activity, identifying patients as candidates to receive a therapeutic that binds to and neutralizes IFN? activity, and in diagnosing or providing a prognosis to patients having IFN?-induced disorders.

Abstract: The present invention encompasses type-I IFN and IFN?-induced PD marker expression profiles, kits, and methods for identifying such IFN?-induced PD marker expression profiles. The type-I IFN and IFN?-induced PD marker expression profiles may also be used in, for example, methods of treating patients having a type-I IFN or IFN?-mediated disorder, methods of monitoring disease progression of patients receiving treatment with a therapeutic agent that binds to and modulates IFN? activity, identifying patients as candidates to receive a therapeutic that binds to and neutralizes IFN? activity, and in diagnosing or providing a prognosis to patients having IFN?-induced disorders.

Abstract: The present invention encompasses type-I IFN and IFN?-induced PD marker expression profiles, kits, and methods for identifying such IFN?-induced PD marker expression profiles. The type-I IFN and IFN?-induced PD marker expression profiles may also be used in, for example, methods of treating patients having a type-I IFN or IFN?-mediated disorder, methods of monitoring disease progression of patients receiving treatment with a therapeutic agent that binds to and modulates IFN? activity, identifying patients as candidates to receive a therapeutic that binds to and neutralizes IFN? activity, and in diagnosing or providing a prognosis to patients having IFN?-induced disorders.

Abstract: Provided herein, in some embodiments, are methods for treating melanoma, improving therapeutic effectiveness of drugs and reducing drug toxicity.

Abstract: The present invention provides anti-human ICOS antibodies with increased effector function. The invention further relates to pharmaceutical compositions, immunotherapeutic compositions, and methods using therapeutic antibodies that bind to the human ICOS antigen and that may mediate ADCC, CDC, and/or antibody-dependent phagocytosis (opsonisation) for the treatment and prevention of T cell-mediated diseases and disorders, such as, but not limited to, chronic infection, autoimmune disease or disorder, inflammatory disease or disorder, graft-versus-host disease (GVHD), transplant rejection, and T cell proliferative disorder.

Abstract: Provided herein are optimized methods for treating a degenerative muscle disease, which comprise determining the presence, absence or amount of a biomarker associated with the disease after a drug has been administered, and determining whether a subsequent dose of the drug should be maintained, increased or decreased based on the biomarker assessment. Increased levels of certain biomarkers are linked to muscle degenerative diseases (e.g., GM-CSF(CSF2), TNF-alpha or other pro-inflammatory cytokine acting through NF kappa B), and decreased levels of certain biomarkers are linked to the muscle degenerative diseases 9 e.g., particular microRNA (e.g., miRNA-1, miRNA-133, miRNA-206)). Such methods optimize therapeutic efficacy and minimize toxicity associated with a drug. Also provided herein are therapeutics for treating muscle disorders.

Abstract: Without limitation, this disclosure relates to compositions and methods for detecting and quantifying the expression of insulin receptor isoform A (IR-A) and/or insulin receptor isoform B (IR-B) in a tissue sample. The disclosure also relates to methods of diagnosis and classification based at least in part upon detecting and quantifying the expression of insulin receptor isoform A (IR-A) and/or insulin B (IR-B) in a tissue sample. Methods of treating a subject based upon such a classification are among additional aspects of the disclosure presented herein.