The present invention relates to a Selective Glucocorticoid Receptor Modulator (SEGRM), or a pharmaceutically acceptable salt thereof, for use in the treatment of impaired skin wound healing in a subject, an in vitro method for identifying a subject suffering from impaired skin wound healing to be responsive to the treatment with a Selective Glucocorticoid Receptor Modulator (SEGRM), or a pharmaceutically acceptable salt thereof, and kits and kits-of-part related thereto.

The present invention relates to methods and compositions for monitoring, diagnosis, prognosis, and determination of treatment regimens in subjects suffering from or suspected of having a renal injury. In particular, the invention relates to using a one or more assays configured to detect a kidney injury marker selected from the group consisting of Thymic stromal lymphopoietin, Vascular endothelial growth factor receptor 1, C-C motif chemokine 1, C-C motif chemokine 17, C-C motif chemokine 21, C-C motif chemokine 27, FLT-3 Ligand, Immunoglobulin G subclass 3, Interleukin-1 receptor type I, Interleukin-20, Interleukin-29, Interleukin-7, Platelet-derived growth factor A/B dimer, Platelet-derived growth factor A/A dimer, and MMP9:TIMP2 complex as diagnostic and prognostic biomarkers in renal injuries.

Bronchial remodelling is a prominent feature of severe asthma and a potential therapeutic target. Some data indicate that Th17 cytokines in particular IL-22 may be involved in remodelling processes in vitro, and in skin remodelling in vivo. The aim of the inventors was to evaluate if Th17 cytokines are involved in bronchial remodelling in a severe model of allergic asthma, and if this was amplified by co-sensitization with NOD2 agonist, MDP, a ligand favouring Th17 polarization. Dog allergen challenge led to a predominant neutrophilic infiltration in Broncho-alveolar lavage (BAL), increased dog-specific IgE production, airways hyperresponsiveness, and increased Th17 cytokine production. Increased bronchial remodeling was observed in dog allergen challenged mice compared to control. IL-22 deficiency decreased airway hyperresponsiveness, bronchial mucus production as well as peribronchial collagen deposition, in the allergen-challenged group. Th17 cytokines in particular IL-22 participate in the bronchial remodeling in a chronic model of neutrophilic asthma, and may represent a therapeutic target in severe asthma.

Among the various aspects of the present disclosure is the provision of a method of treating an inflammatory bowel disease. Another aspect provides the provision of a screening method for therapeutic agents. Another aspect provides a method of detecting T.sub.reg cells to determine if a subject has an inflammatory disease. The present disclosure provides for methods of treatment, diagnosis, and screening for drugs for colitis and ileitis.

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

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

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.

Diagnostic screening tests that can be used to identify if a patient is a good candidates for an implantable vagus nerve stimulation device. One or more analyte, such as a cytokine or inflammatory molecule, can be measured from a blood sample taken prior to implantation of a vagus nerve stimulator to determine the patient's responsiveness to VNS for treatment of an inflammatory disorder.