The invention features methods and compositions that are useful for the treatment of diseases, disorders, conditions, or injuries characterized by insufficient myelination. The methods involve administering GPR17 antagonists and microglia inhibitors or ablation agents.

The current disclosure relates to methods for treating ovarian cancer based on specific antigen expression of the cancer. Furthermore, the expressed antigen may be used in immunotherapeutic methods for treatment of the ovarian cancer. Aspects of the disclosure relate to immunotherapies targeting CT45 polypeptides, methods for treating ovarian cancer based on CT45 expression, and kits for detecting CT45 polypeptides and nucleotides.

The present invention relates to compositions and methods for preparing in vitro models of non-alcoholic fatty liver disease, and more particularly of liver steatosis and fibrosing non-alcoholic steatohepatitis (NASH).

The present disclosure provides compositions comprising anti-LMP2 TCR-T cell populations for the treatment of EBV-associated cancers and methods of making and using same.

Compositions and methods are provided for converting the predominant circulating classical monocytes to a non-classical and/or intermediate monocyte phenotype through cytokine stimulation via, for example, macrophage colony-stimulating factor. Once cultured into dendritic cells, these non-classical and/or intermediate monocyte derived cells have increased costimulatory molecule expression, which leads to improved immune and clinical responses in cancer patients receiving dendritic cell vaccination and other immunotherapies. In addition, assays and diagnostic and theranostic methods are provided herein that relate to the discoveries that, prior to treatment, intermediate (CD14+CD16+) and non-classical (CD14dimCD16+) monocytes are increased more than two-fold in patients who later had complete responses to dendritic cell therapy or DC vaccination.

In some embodiments, compositions and methods relating to isolated artificial antigen presenting cells (aAPCs) are disclosed, including aAPCs comprising a myeloid cell transduced with one or more viral vectors, such as a MOLM-14 or a EM-3 myeloid cell, wherein the myeloid cell endogenously expresses HLA-AB/C, ICOS-L, and CD58, and wherein the one or more viral vectors comprise a nucleic acid encoding CD86 and a nucleic acid encoding 4-1BBL and/or OX40L and transduce the myeloid cell to express CD86 and 4-1BBL and/or OX40L proteins. In some embodiments, methods of expanding tumor infiltrating lymphocytes (TILs) with aAPCs and methods of treating cancers using TILs after expansion with aAPCs are also disclosed.

The invention features methods of producing compositions enriched in Tregs and methods for treating immunological disorders using these compositions. The invention also features methods for producing compositions enriched in lymphocytes and depleted of Tregs and the use of these compositions in the treatment of proliferative disorders.

The description discloses a device and a kit adapted for selection of cells that are resistant to receptor-mediated apoptosis and a method for using the device and kit. The device enables negative selection of mature immune cells which induce graft versus host disease (GvHD) out of a heterogeneous cell population which is introduced into the device. The device enables an efficient cell selection in simplified and cheaper setting by an off the shelf product—a solution that currently do not exist. The description further discloses uses for the device.

The current invention concerns isolated liver progenitor cells, cell lines thereof, cell populations comprising such and compositions comprising such wherein the liver progenitor cells are HLA-E positive. In addition, the invention concerns methods of preparing these liver progenitor cells.

The invention relates to an in vitro method to generate T cell progenitors, comprising the step of culturing CD34+ cells in a medium containing TNF-alpha and/or an antagonist of the Aryl hydro-carbon/Dioxin receptor, in particular StemRegenin 1 (SR1), in presence of a Notch ligand and optionally a fibronectin fragment.