Human umbilical cord blood-derived monocytes that markedly promote A clearance through heterodimerization of sAPP with A and resultant sAPP production for prevention or treatment of Alzheimer's disease and other neurodegenerative disorders (including stroke and TBI). It was discovered that multiple low-dose infusions of human umbilical cord blood cells (HUCBCs) ameliorate cognitive impairments and reduce A-associated neuropathology in PSAPP transgenic mice, which markedly promotes amyloid precursor protein (APP) -cleavage and resultant sAPP production for pharmaceutical purposes, in particular for treating or slowing the progression of Alzheimer's disease.

T cells harvested from an ALS patient are subjected to a de-differentiation and re-differentiation process to yield T.sub.REG/Th2 hybrid T cells and are then administered to the ALS patient as a cell therapy. The harvested T cells are first cultured in medium containing vitamin D, temsirolimus, and an IL-2 signaling inhibitor to de-differentiate the cells and then the de-differentiated cells are then transferred to a culture medium with IL-2, IL-4, and TGF-.

Peptides that generate an immune response to glioma-related H3.3 proteins and methods of their use are provided.

The present disclosure provides methods for treating ALS using pentostatin and cyclophosphamide treatment followed by T.sub.REG and/or T.sub.REG/Th2 hybrid cells from de-differentiated T cells. The present disclosure further provides methods for producing T.sub.REG and T.sub.REG/Th2 hybrid cells from de-differentiated T cells, said T.sub.REG and T.sub.REG/Th2 hybrid cells, populations thereof and compositions thereof. Methods for producing de-differentiated T cells, said de-differentiated T cells, populations thereof and compositions thereof are also provided.

In one aspect, the invention provides a composition comprising at least one monocyte comprising an agent that increases monocyte homing to a site of injury, and an effective amount of a drug. In another aspect, the invention provides a method of using the composition to deliver a drug to a site of injury.

The present invention relates to compositions and methods for treating diseases, disorders or conditions associated with the expression of the glycosyl-phosphatidylinositol (GPI)-linked GDNF family protein -receptor 4 (GFR4).

The invention provides compositions and methods for suppressing autoimmune components of neurodegenerative diseases and thereby providing therapeutic effects to patients suffering from such diseases. Compositions and methods include immunosuppressive moieties such as regulatory T cells (Tregs) and proteins expressed by Tregs coupled to a chimeric antigen receptor or protein that specifically binds one or more glial cell markers. Therapeutically effective doses of said compounds for treating neurodegenerative diseases including progressive supranuclear palsy (PSP), Parkinson's disease (PD), Alzheimer's, Huntington's disease, amyotrophic lateral sclerosis (ALS), chronic traumatic encephalopathy (CTE), and prion diseases are disclosed.

The present disclosure generally relates to novel chimeric antigen receptors (CARs), modified regulatory T cells (Tregs) expressing such CARs and/or Tregs which are engineered to express neurodegenerative disease modifying molecules, e.g., which express molecules which prevent oxidative/inflammatory activity, or which promote neuronal growth/survival such as nerve growth factors or non-classical neurotrophic factors. The present disclosure also generally relates to compositions containing such modified Tregs, and methods of use thereof as therapeutics, in particular for treating and preventing neurodegenerative diseases and symptoms associated with therewith, and/or for slowing the onset of such neurodegenerative diseases, particularly in persons at risk because of genetic factors or in persons exhibiting early signs of developing such a neurodegenerative disease.

The present invention generally relates to the field of genome engineering (gene editing), and more specifically to ex vivo gene therapy for the treatment of Activated PI3kinase Delta Syndrome type 1 (APDS1) related to PIK3CD gene. Particularly, the present invention pertains to the treatment of PIK3CD deficiency in hematopoietic stem cells (HSCs) and/or T-cells. The present invention provides means and methods for genetically modifying HSCs and/or T-cells involving gene editing reagents, such as TALE-nucleases, that specifically target an endogenous PIK3CD locus, at least in the PIK3CD allele comprising at least one APDS1-associated mutation, thereby allowing the restoration of the normal cellular phenotype. The present invention also provides engineered PIK3CD-edited HSCs and engineered PIK3CD-edited T-cells comprising at least one exogenous sequence comprising a nucleic acid sequence encoding a functional PI3K protein which is integrated in said HSCs' or T-cells' genome into a PIK3CD locus, in a non-functional PIK3CD allele, resulting in the expression of a functional PI3K polypeptide. The present invention further provides populations of cells comprising said engineered HSCs or T-cells, pharmaceutical compositions comprising said engineered cells or populations of cells, as well as their use in gene therapy for the treatment of APDS1.

In one aspect, the invention provides a composition comprising at least one monocyte comprising an agent that increases monocyte homing to a site of injury, and an effective amount of a drug. In another aspect, the invention provides a method of using the composition to deliver a drug to a site of injury.