The present invention relates to the screening, diagnosis, prognostic evaluation, and treatment or prevention of age associated inflammation, chronic inflammation, and inflammatory diseases. In particular, the present invention relates to treating or preventing inflammatory diseases (e.g. rheumatoid arthritis or spondyloarthritis) or patients with inflammatory peripheral GnRH with GnRH antagonists or drugs that lower the effects of GnRH.

Compositions and methods of treating an inflammatory disease in a subject are provided. Accordingly there is provided a method comprising administering to the subject a therapeutically effective amount of an agent which selectively inhibits activity and/or expression of iron regulatory protein (IRP) 1 and not IRP2, thereby treating the inflammatory disease in the subject. Also provided is a pharmaceutical composition comprising, as an active ingredient, an agent which selectively inhibits activity and/or expression of IRP1 and not IRP2, and a pharmaceutically acceptable carrier or excipient. Also provided are methods of identifying an agent that selectively modulates an activity of an IRP member of an IRP family of polypeptides and not of an additional IRP member of said IRP family of polypeptides.

Antibodies against citrullinated protein antigens (ACPA) have shown their relevance for the diagnosis and possibly pathogenesis in arthritis. Described are means and methods for determining antibodies against homocitrulline-containing proteins or carbamylated proteins/peptides (anti-CarP) for the classification of individuals suffering from, or at risk of suffering from, arthritis.

The present disclosure provides for compositions and methods for identifying peptide classifiers. In one embodiment, a peptide classifier for diagnosing rheumatoid arthritis includes a composition comprising a plurality of molecules. Each molecule comprises a peptide having a sequence selected from SEQ ID NOS: 1-8861, wherein the plurality of molecules defines a classifier for rheumatoid arthritis.

The invention relates to method of diagnosis a subject suffering from Adult-onset Still's disease and further to determine the disease course of the subject suffering from Adult-onset Still's disease.

The present invention relates generally to methods for diagnosing the presence or the risk of development or the therapy control of spondyloarthritis (Spa), in particular, of ankylosing spondylitis (AS) and undifferentiated spondyloarthritis in a subject, in particular in mammals. In addition, the present invention relates to test kits for use in the diaposis of the presence or the risk of development, or for the therapy control of Spa, like AS and undifferentiated spondyloarthritis, in a subject. In particular, the present invention relates to a method for diagnosing the presence or the risk of development, or for the therapy control of Spa, like AS and undifferentiated spondyloarthritis, it a subject analysing for the presence of autoantibodies against CD74 and/or IKBKB in a subject. The presence of autoantibodies against CD74 and/or IKBKB is indicative for the presence or the risk of development, or for the therapy control of Spa, like AS and undifferentiated spondyloarthritis. In particular, detection of the presence of autoantibodies against CD74 and/or IKBKB allows early diagnostic of Spa, in particular, AS and undifferentiated spondyloarthritis.

The relates to the field of diagnosis and treatment of Rheumatoid Arthritis, in particular of assessing responsiveness of rheumatoid arthritis patients to biological treatment. In particular the it has been found that measurement of MDR1 and/or MRP1 transport activities in the early phase of or before a bDMARD treatment is appropriate to provide a prediction on the effectiveness or success of bDMARD therapy once csDMARD therapy has failed. Thus, the invention relates to an in vitro diagnostic method for assessing the responsiveness of a sDMARD treated RA patient to bDMARD therapy, wherein preferably the patient is in need of a switch or modification of the sDMARD therapy by measuring transport activities of the above-mention transporters or their composite activities. The invention also relates to use of kits for the methods of the invention and methods for treatment comprising the diagnosis or prediction of the invention.

An isoform of the TGF beta receptor II comprising a sequence of about of 80 amino acids and lacking a transmembrane domain. The isoform comprises the amino acid sequence set forth in SEQ ID No. 12. The isoform may have the amino acid sequence set forth in SEQ ID No. 2 or sequences having at least 85% sequence identity to the sequence set forth in SEQ ID No. 2. A fusion peptide is provided comprising an isoform of the TGF beta II receptor fused to a ligand, wherein a vector comprising the fusion peptide is used to treat cancer and/or hepatic fibrosis. An antibody binding the soluble isoform of the TGF beta II receptor is provided. The antibody binds the amino acid sequence shown in SEQ ID No. 12 and is used in in vitro methods.

An in vitro method for diagnosis, prognosis, risk assessment, monitoring, therapy guidance and/or therapy control of an infectious disease, includes (a.) providing a sample of a subject exhibiting clinical symptoms of and/or suspected of having an infection, (b.) determining a level of D-lactate in said sample, (c.) in which the level of D-lactate is indicative of the presence of an infectious disease, characterized in that (d.) the level of D-lactate in said sample is determined by means of an electrochemical sensing system (biosensor). In embodiments, the electrochemical sensing system includes a potentiometric or an amperometric sensor. Preferably, the electrochemical system includes a D-lactate binding molecule, that is preferably immobilized on a detection (working) electrode. In embodiments, the detection electrode with the immobilized D-lactate binding molecule is included by a (disposable) test strip for insertion into a portable reader.

An object of the present invention is to provide a method for predicting a therapeutic effect of a drug that inhibits FKN-CX3CR1 interaction on rheumatoid arthritis in a rheumatoid arthritis subject, and novel and more effective therapeutic agent for rheumatoid arthritis exploiting the method. In order to predict a therapeutic effect of a drug that inhibits fractalkine (FKN)-CX3CR1 interaction in a rheumatoid arthritis subject, provided is a method comprising predicting the therapeutic effect of the drug in the subject on the basis of a measurement value of CD16+ monocytes in a biological sample obtained from the subject before the start of administration of the drug.