A method of determining a pharmacodynamics or pharmacokinetic effect of an inhibitor of IL 1α comprising providing a sample from a subject; administering the inhibitor of IL 1α to the sample; measuring levels of one or more biomarkers in the sample; and determining the pharmacodynamic or the pharmacokinetic effect of the inhibitor of IL 1α based on the levels of the one or more biomarkers.

The invention provides methods and systems for detecting a biomarker in a synovial fluid wherein the system also includes a control to ensure that the test sample is indeed synovial fluid. The biomarkers and the control for synovial fluid can be identified using proteomic methods, including but not limited to antibody based methods, such as an enzyme-linked immunosorbant assay (ELISA), a radioimmunoassay (RIA), or a lateral flow immunoassay.

The invention provides methods and systems for detecting a biomarker in a synovial fluid wherein the system also includes a control to ensure that the test sample is indeed synovial fluid. The biomarkers and the control for synovial fluid can be identified using proteomic methods, including but not limited to antibody based methods, such as an enzyme-linked immunosorbant assay (ELISA), a radioimmunoassay (RIA), or a lateral flow immunoassay.

The invention provides anti-CD30 antibody-drug conjugates, such as brentuximab vedotin, and their use for the treatment of lymphoma, such as diffuse large B-cell lymphoma. The invention also provides the use of anti-CD30 antibody-drug conjugates, such as brentuximab vedotin, in combination with lenalidomide and/or anti-CD20 antibodies, such as rituximab, for the treatment of lymphoma, such as diffuse large B-cell lymphoma.

Disclosed are methods of isolating a TCR having antigenic specificity for a mutated amino acid sequence encoded by a cancer-specific mutation, the method comprising: identifying one or more genes in the nucleic acid of a cancer cell of a patient, each gene containing a cancer-specific mutation that encodes a mutated amino acid sequence; inducing autologous APCs of the patient to present the mutated amino acid sequence; co-culturing autologous T cells of the patient with the autologous APCs that present the mutated amino acid sequence; selecting the autologous T cells; and isolating a nucleotide sequence that encodes the TCR from the selected autologous T cells, wherein the TCR has antigenic specificity for the mutated amino acid sequence encoded by the cancer-specific mutation. Also disclosed are related methods of preparing a population of cells, populations of cells, TCRs, pharmaceutical compositions, and methods of treating or preventing cancer.

The present disclosure provides materials and methods for determining the presence of an N-terminal modification on a therapeutic protein, and/or the efficiency of N-terminal modification, such as PEGylation, at the N-terminus of a therapeutic protein such as Filgrastim (wherein the PEGylated version is therefore Pegfilgrastim).

Methods of selecting test compounds on the basis of their cellular response profiles are disclosed. For a given test compound, a cellular response is determined by introducing into an array of individually addressable microwells a population of cells comprising a plurality of cell types and contacting the cells with the test compound. The cellular response profile for the test compound is then compared to a desired cellular response profile, and the test compound is selected based on the comparison.

Disclosed are methods of isolating a TCR having antigenic specificity for a mutated amino acid sequence encoded by a cancer-specific mutation, the method comprising: identifying one or more genes in the nucleic acid of a cancer cell of a patient, each gene containing a cancer-specific mutation that encodes a mutated amino acid sequence; inducing autologous APCs of the patient to present the mutated amino acid sequence; co-culturing autologous T cells of the patient with the autologous APCs that present the mutated amino acid sequence; selecting the autologous T cells; and isolating a nucleotide sequence that encodes the TCR from the selected autologous T cells, wherein the TCR has antigenic specificity for the mutated amino acid sequence encoded by the cancer-specific mutation. Also disclosed are related methods of preparing a population of cells, populations of cells, TCRs, pharmaceutical compositions, and methods of treating or preventing cancer.

The present invention concerns markers of multiple sclerosis, their use, and treatment with IL-17 antagonists, including IL-17 antibodies, of subjects with increased levels of such markers.

Disclosed herein is a T-helper cell (“T.sub.H-GM” cell) that is regulated by IL-7/STAT5 and which secrete GM-CSF/IL-3. Also disclosed are methods and compositions for modulating T.sub.H-GM function for the treatment of, e.g., inflammatory disorders. Diagnostic and prognostic methods for specifically identifying T.sub.H-GM-mediated inflammatory disorders (e.g., rheumatoid arthritis), as distinct from and/or in addition to non-T.sub.H-GM-mediated (e.g., TNF-α-mediated) inflammatory disorders, are also provided.