The technology relates in part to methods for detecting the activity of Meteorin-β and modified versions thereof.

The present invention relates to methods and compositions for monitoring, diagnosis, prognosis, and determination of treatment regimens in stroke patients and in patients at risk for stroke. In particular, the invention relates to using assays that detect one or more biomarkers as diagnostic and prognostic biomarker assays in such patients.

Engineered multivalent and multispecific binding proteins, methods of making, and their uses in the prevention, diagnosis, and/or treatment of disease are provided.

Methods using biomarkers, e.g., serum levels of ST2, to predict risk of developing hypertension, as well as methods for treating subjects to reduce the risk of developing hypertension and methods for selecting and/or stratifying subjects for clinical trials of treatments to reduce the risk of hypertension.

The present invention pertains to an N-terminally truncated interleukin (IL)-38 protein, or functional variants thereof, as well as to nucleic acids and vectors encoding the truncated IL-38 peptide and recombinant cells comprising these nucleic acids or vectors. The invention shows that IL-38 is N-terminally processed and that the truncated version of the cytokine acts as an antagonist of immune activation in macrophages. This indicates a use of the truncated cytokine in the treatment and prevention of autoimmune disorders. The invention further provides pharmaceutical compositions comprising the truncated IL-38 protein, and method for screening modulators of the function of truncated IL-38.

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.

Disclosed herein are engineered monovalent binding proteins that bind to one or more antigens, as well as methods of making and using the binding proteins in the prevention, diagnosis, and/or treatment of disease.

The present invention provides methods for predicting clinical outcome from a sample of a subject having ulcerative colitis (UC), comprising determining a prognostic marker profile and classifying the subject as either a responder or a non-responder. The methods can be used to monitor and to predict the progression of UC, by determining the likelihood for UC to progress either rapidly or slowly in an individual based on the presence or level of at least one marker in a sample. The methods can also be used to predict the regression of UC, by determining the likelihood for UC to regress either rapidly or slowly in an individual.

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.

A compound comprising, in combination: a cell surface binding ligand or internalizing factor, such as an IL-13Rα2 binding ligand; at least one effector molecule (e.g., one, two, three or more effector molecules); optionally but preferably, a cytosol localization element covalently coupled between said binding ligand and said at least one effector molecule; and a subcellular compartment localization signal element covalently coupled between said binding ligand and said at least one effector molecule (and preferably with said cytosol localization element between said binding ligand and said subcellular compartment localization signal element). Methods of using such compounds and formulations containing the same are also described.