The invention relates to a method for detecting and measuring the presence of nucleosome-protein adducts and the use of such measurements for the detection and diagnosis of disease. The invention also relates to a method of identifying nucleosome adduct biomarkers for the detection and diagnosis of disease and to biomarkers identified by said method.

Novel means that enables prediction of prognosis of a patient with cancer or inflammatory disease is disclosed. In the method for prediction of prognosis of a patient with cancer or inflammatory disease according to the present invention, the expression level of the FROUNT gene in a sample collected from the patient is measured. Since FROUNT is a poor prognostic factor, the lower the expression level of the FROUNT gene is, the better the prognosis in the patient is predicted to be. Or, the expression level of the CC chemokine receptor/ligand gene in a sample collected from the patient is measured. Since the CC chemokine receptor/ligand gene such as CCR2 or CCR5 is a good prognostic factor, the higher the expression level of the CC chemokine receptor/ligand gene is, the better the prognosis in the patient is predicted to be.

There is provided a method of evaluating risk of severe outcome of an infectious disease and/or an inflammatory disease in a patient, the method comprising: determining/measuring the number of one or more immune cells selected from the group consisting of VD2 T cells, CD8 T cells, and immature neutrophils in a sample obtained from the patient, wherein the patient has an enhanced risk of severe infectious disease and/or inflammatory disease outcome when: (i) the ratio of immature neutrophils to VD2 T cell is at least 2:1, and/or (ii) the ratio of immature neutrophils to CD8 T cell is at least 0.5:1. Also disclosed are method of treating a patient with a severe infectious disease and/or inflammatory disease and kit for use in methods thereof.

A method of treating an inflammatory disorder in a subject, comprising administering to a subject in need thereof a nucleic acid molecule for inhibiting the expression of Hom-1.

An in-vitro method for the prediction, prognosis and/or diagnosis of an inflammatory response associated with a condition or disease such as schizophrenia in a subject, the method comprising determining in a sample of a subject the level of 25-hydroxy vitamin D3, preferably in combination with the level of least one biomarker wherein the at least one biomarker is selected from innate chemokine (IL-8) and matrix metalloproteinase (MMP-9); and comparing the levels of said 25-hydroxy vitamin D3 and at least one biomarker to a control level of 25-hydroxy vitamin D3 and the at least one biomarker respectively in order to determine a positive or negative prediction, prognosis and/or diagnosis of said inflammatory response indicating an associated condition or disease, such as schizophrenia.

The present invention relates to a panel of inflammasone biomarkers for detecting exposure to ionizing radiation and/or for determining absorbed dose of ionizing radiation in a subject exposed thereto.

The presently disclosed subject matter provides compositions, kits, and methods comprising imaging agents that can detect Programmed Cell Death Ligand 1 (PD-L1). The presently disclosed imaging agents can be used to detect diseases and disorders, such as cancer, infection, and inflammation, in a subject.

Provided herein are methods and kits for analyzing a biological sample obtained from a subject having, suspected of having, or being at risk for a disease associated with the contact activation system.

The present invention is directed toward novel methods to identify as well as to treat a subject having an inflammatory disease resistant to corticosteroids.

Interleukin (IL)-33 is a critical regulator of allergic airway inflammation in the lung and is released by stressed or damaged epithelial cells. Here, Applicants show that alveolar macrophages regulate epithelial alarmin expression via CLEC-2 (C-type Lectin-like Receptor-2), which binds to PDPN (podoplanin). Therefore, CLEC-2/PDPN interactions are critical for regulating type 2 immunity in the lung and modulating expression of the epithelial alarmin IL-33. Methods are disclosed for therapeutic and screening applications. Novel therapeutic targets in alveolar macrophages and epithelial cells are disclosed.