Systemic Lupus Erythematosus is marked by altered immune regulation linked to waxing and waning clinical disease. Embodiments described herein identify sets of biomarkers/mediators and their use for informing and/or predicting a future SLE disease activity event such as an impending SLE flare or SLE-related organ inflammation. Such an approach can be beneficial in the management of lupus.

In one aspect, a system for detecting inflammation is disclosed, which includes at least one sensor comprising at least one port for receiving a biological sample, and at least one electrochemical cell in fluid communication with said at least one port for receiving said biological sample, said electrochemical cell comprising at least two electrically conductive electrodes, where at least one of said electrodes is functionalized with at least one probe exhibiting specific binding to at least one inflammation biomarker. The system may further include a circuitry for detecting a redox current flowing through said at least one electrode and/or an electrical impedance across said electrodes in response to interaction of the functionalized electrode with the sample, and generating signals in response to said detection. By way of example, the biological sample can be a subject's blood serum.

The invention provides biomarkers for predicting the response to checkpoint inhibitors. The inventors demonstrate that a PD-1/PD-L1 inhibitor exerts antitumor activity against tumor with low PD-L1 expression and immune-desert phenotype through blocking PD-L1 in the lymph nodes. The invention provides novel combinations of intratumoral markers for antigen cross-presenting cells and T cell chemokines which are expected to be superior efficacy-predicting biomarkers compared to existing methods.

A method for predicting sepsis or diagnosing systemic inflammatory response syndrome (SIRS) and/or sepsis in a subject comprises determining levels of at least three markers selected from CCL23, A1AT, CRP, sICAM, PLA2, IL-6, procalcitonin, MMP8, TNFalpha, AcPGP, enzymatic MMP activity, TIMP1, sRAGE and desmosine in a sample taken from the subject. The combined levels of the at least three markers are used to predict or diagnose SIRS and/or sepsis. The methods may be performed on a subject with SIRS and which is used to identify an infection in the subject. A preferred panel of markers includes CCL23, A1AT, sICAM, sICAM/VCAM-1 and CRP. Corresponding products, methods of treatment and medical uses are provided.

A novel cytokine, U83A, is described, as are variant forms of the cytokine, having a wide range of agonistic and antagonistic activity against chemokine receptors. Uses of the chemokine in treatment of a range of diseases, including cancers and HIV/AIDS, are described.

A method for predicting whether a patient will be a long-term survivor on treatment of a disease by adoptive cell transfer (ACT), is disclosed comprising: (i) analysing a blood-derived sample obtained from the patient for one or more prognostic markers of long-term survival on treatment of a disease by ACT, and; (ii) based on the analysis of step (i), predicting whether the patient will be a long-term survivor on treatment of the disease by ACT. Also disclosed are methods for treating a patient by ACT, methods for selecting a patient for treatment by ACT, and methods for selecting a patient for treatment of a disease by ACT.

The present invention relates to an assay for determining endogenous levels of analyte in vivo. In particular, the present invention is directed to an assay for determining endogenous levels of stromal cell-derived factor (SDF-1) isoforms in vivo.

The invention relates to panels of biomarkers for diagnosing and/or monitoring the progression of an active mycobacterial infection or for diagnosing the absence of a mycobacterial infection, particularly tuberculosis. Such diagnosis and/or monitoring may be differential diagnosis between active tuberculosis patients and patients with latent, non-progressing tuberculosis or healthy or sick patients, irrespective of whether the patients have been characterised as being sputum smear positive or sputum smear negative, and/or irrespective of whether they have been characterised as being HIV positive or HIV negative. The above pertain in all aspects both to pulmonary and extra pulmonary Mycobacterium tuberculosis infections, with Mycobacterium tuberculosis being the causative organism in tuberculosis.

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.

Methods of treating IBD in a subject using an anti-SMAD7 therapy, such as a SMAD7 antisense oligonucleotide, to reduce CCL20, IL8, or TNFα levels are disclosed. Methods of treating and managing IBD in a subject using an anti-SMAD7 therapy, such as a SMAD7 antisense oligonucleotide, based on CCL20, IL8, or TNFα levels are also disclosed. Also disclosed are methods of determining whether a subject with IBD is responsive or likely to be responsive to treatment an anti-SMAD7 therapy. Reduction of CCL20, IL8, or TNFα levels may correlated with IBD remission or decreases in CDAI score.