Abstract: The present invention relates to a method of reducing the numbers of eosinophils in a human subject comprising administration to a subject an IL-5R binding molecule that comprises (a) a region that specifically binds to the IL-5R and (b) an immunoglobulin Fc region. In a specific embodiment, a method of the invention reduces the number of eosinophils in blood, bone marrow, gastrointestinal tract (e.g. esophagus, stomach, small intestine and colon), or lung.

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 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 relates to a method of reducing the numbers of eosinophils in a human subject comprising administration to a subject an IL-5R binding molecule that comprises (a) a region that specifically binds to the IL-5R and (b) an immunoglobulin Fc region. In a specific embodiment, a method of the invention reduces the number of eosinophils in blood, bone marrow, gastrointestinal tract (e.g. esophagus, stomach, small intestine and colon), or lung.

Abstract: The present invention relates to a method of reducing the numbers of eosinophils in a human subject comprising administration to a subject an IL-5R binding molecule that comprises (a) a region that specifically binds to the IL-5R and (b) an immunoglobulin Fc region. In a specific embodiment, a method of the invention reduces the number of eosinophils in blood, bone marrow, gastrointestinal tract (e.g. esophagus, stomach, small intestine and colon), or lung.

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 relates to a method of reducing the numbers of eosinophils in a human subject comprising administration to a subject an IL-5R binding molecule that comprises (a) a region that specifically binds to the IL-5R and (b) an immunoglobulin Fc region. In a specific embodiment, a method of the invention reduces the number of eosinophils in blood, bone marrow, gastrointestinal tract (e.g. esophagus, stomach, small intestine and colon), or lung.

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 prognoses to patients having IFN?-induced disorders.

Abstract: The present invention relates to a method of reducing the numbers of eosinophils in a human subject comprising administration to a subject an IL-5R binding molecule that comprises (a) a region that specifically binds to the IL-5R and (b) an immunoglobulin Fc region. In a specific embodiment, a method of the invention reduces the number of eosinophils in blood, bone marrow, gastrointestinal tract (e g, esophagus, stomach, small intestine and colon), or lung.

Abstract: The present invention relates to a method of treating SLE in a human subject comprising administration of an anti-interferon ? antibody.

Abstract: The present invention relates to methods of treating, preventing or preventing the progression of fibrosis comprising inhibiting the actions of pulmonary and activation-regulated chemokine (PARC) or at least one of its downstream effector molecules, such as Sp1 transcription factor and protein kinase C-alpha (PKC?). The present invention also relates to methods of screening and/or identifying compounds useful for the treatment of fibrosis comprising contacting PARC or its downstream effector molecules, such as Sp1 or PKC?, with a substance and subsequently determining the effects of the substance on the activity of PARC or Sp1 or PKC?. The present invention also relates to methods of screening and/or identifying compounds that prevent or inhibit collagen deposition comprising contacting PARC or its downstream effector molecules, such as Sp1 or PKC?, with a substance and subsequently determining the effects of the substance on the activity of PARC or Sp1 or PKC?.