It is described in vitro methods for expanding, detecting or isolating rare populations of antigen specific memory T cells. It is also described an in vitro method for obtaining a genetically modified memory T cell population. Uses of cells so obtained are also disclosed.

The invention relates to methods for predicting the in vivo nephrotoxicity of a drug substance, in particular a nucleic acid molecule such as a siRNA or an antisense oligonucleotide using an in vitro cell based assay measuring the levels of extracellular EGF as toxicity biomarker, potentially in combination with other biomarkers like ATP and KIM-1.

This invention relates generally to compositions and methods for identifying the regulatory network that modulates, controls or otherwise influences T cell balance, for example, Th17 cell differentiation, maintenance and/or function, as well compositions and methods for exploiting the regulatory network that modulates, controls or otherwise influences T cell balance in a variety of therapeutic and/or diagnostic indications. This invention also relates generally to identifying and exploiting target genes and/or target gene products that modulate, control or otherwise influence T cell balance in a variety of therapeutic and/or diagnostic indications.

This invention relates to methods for predicting a prognosis of a patient with cancer in need of an anti-cancer treatment comprising measuring a cytokine score from a sample obtained from the patient. In some embodiments, the subject is administered an anti-cancer treatment, e.g., an anti-PD-1 antibody, following the cytokine score measurement. In some embodiments, the cancer is lung cancer.

The present invention relates to a tumor necrosis factor receptor (TNFR) binding protein complex comprising 12 or more N protein ligands (PLs) that specifically bind to the extracellular part of the same TNFR. Preferably, the TNFR binding protein complex binds to the extracellular part of TNFR2. Preferably, the TNFR binding protein complex of the present invention further comprises a two or more polymerization domains (PD).

Adult-onset leukoencephalopathy with axonal spheroids and pigmented glia (ALSP) is caused by dominant inactivating mutations in the colony stimulating factor receptor 1 (CSF1R) kinase domain. GM-CSF haploinsufficiency corrects olfactory, cognitive and emotional functions lost in Csf1r+/− mice. This correlates with the correction of microgliosis and microglial functions resulting in improvement of myelination and rescue of neurogenesis. However, GM-CSF haploinsufficiency fails to correct the motor deficits of Csf1r+/− mice and cerebellar microgliosis. The present invention discloses methods and compositions using GM-CSF as a suitable therapeutic target to inhibit in amelioration of the cognitive impairments in ALSP and other in conditions involving inflammatory activation of microglia and macrophages, such as AD, ALS, multiple sclerosis, and hippocampal inflammation following radiation therapy. Treatment with GM-CSF inhibitors is beneficial in ALSP, as adult neurogenesis is important for memory, olfaction and prevention of anxiety/depression and early initiation of such treatment in carriers of CSF1R mutations may increase effectiveness. Balancing the actions of CSF-1R and GM-CSF signaling are necessary to preserve olfaction, cognition and emotional balance in aged mice. This balance is likely altered in many neurodegenerative diseases in which activated microglia contribute to the pathology.

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 includes a composition and a method of modulating an immune response with a composition that comprises an anti-BAFF receptor antibody or binding fragment thereof that is bound or conjugated to an siRNA, and shRNA, or both, that targets a BAFF receptor mRNA.

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.

Presented herein are systems and methods for developing classifiers useful for predicting response to particular treatments. For example, in some embodiments, the present disclosure provides a method of treating subjects suffering from an autoimmune disorder, the method comprising a step of: administering an anti-TNF therapy to subjects who have been determined to be responsive via a classifier established to distinguish between responsive and non-responsive prior subjects in a cohort who have received the anti-TNF therapy.