The present disclosure relates generally to compositions for inducing an immunosuppressive phenotype in an antigen presenting cell of the immune system via ligands that activate CD1d signaling. Uses thereof in a therapeutic protocol for treating or preventing conditions associated with aberrant immune system activation, such as autoimmune disease, inflammatory disease, allergy and transplant rejection are detailed.

The present disclosure relates generally to compositions for inducing an immunosuppressive phenotype in an antigen presenting cell of the immune system via ligands that activate CD1d signaling. Uses thereof in a therapeutic protocol for treating or preventing conditions associated with aberrant immune system activation, such as autoimmune disease, inflammatory disease, allergy and transplant rejection are detailed.

The present invention provides preparations of MSCs with important therapeutic potential. The MSC cells are non-primary cells with an antigen profile comprising less than about 1.25% CD45+ cells (or less than about 0.75% CD45+), at least about 95% CD105+ cells, and at least about 95% CD166+ cells. Optionally, MSCs of the present preparations are isogenic and can be expanded ex vivo and cryopreserved and thawed, yet maintain a stable and uniform phenotype. Methods are taught here of expanding these MSCs to produce a clinical scale therapeutic preparations and medical uses thereof.

Compounds with the following structures ##STR00001##
and their analogs are provided. Compositions that include these structures can be used to inhibit glucose transporters and stop or decrease the proliferation of cancer, treat possible organ rejection and treat autoimmune disease.

Compositions of genetically modified beta-like cells are encompassed. Also encompassed are methods of treatment of type 1 diabetes using these compositions or compositions that inhibit the function of the identified genes.

The present invention relates to immunoglobulins that bind FcγRIIb+ cells and coengage the antigen on the cell's surface and an FcγRIIb on the cell's surface, methods for their generation, and methods for using the immunoglobulins.

The present disclosure relates to methods for increasing telomere length in one or more human cells and/or increasing genome stability of one or more human cells, for example by contacting one or more human cells with an agent that increases expression of Zscan4 in the one or more human cells. Methods of treating a subject in need of telomere lengthening, treating a disease or condition associated with a genomic and/or chromosome abnormality, of rejuvenating one or more human cells, of rejuvenating tissues or organs, and of rejuvenating a subject in need thereof, for example by contacting one or more human cells in the subject with an agent that increases expression of Zscan4, or by administering to a subject in need thereof, an agent that increases expression of Zscan4 are also provided.

It is intended to provide MSCs for transplantation that have an improved post-transplantation cell survival rate and engraftment rate and are highly safe with fewer adverse reactions, and a method for conveniently producing MSCs for transplantation having a high cell survival rate and engraftment rate. As means therefor, the present invention provides a stem cell for transplantation comprising an MSC capable of overexpressing IL-10.

The present invention relates to novel antibodies, in particular murine monoclonal antibodies, chimeric and humanized, that are able to block specifically the human IgG receptors FcγRIIIA (CD16A) and FcγRIIIB (CD16B) as well as the amino and nucleic acid sequences coding for such antibodies. The invention also comprises the use of such antibodies or of fragments thereof as a medicament for the preventive and/or therapeutic treatment of diseases involving CD16, like autoimmune diseases, inflammatory disorders, allergies and infections, without inducing any adverse effects. In particular, these antibodies and fragments can prevent or treat anti-drug idiopathic thrombocytopenic purpura (ITP), rheumatoid arthritis (RA) and autoimmune hemolytic anemia (ANA).

The present invention relates to novel antibodies, in particular murine monoclonal antibodies, chimeric and humanized, that are able to block specifically the human IgG receptors FcγRIIIA (CD16A) and FcγRIIIB (CD16B) as well as the amino and nucleic acid sequences coding for such antibodies. The invention also comprises the use of such antibodies or of fragments thereof as a medicament for the preventive and/or therapeutic treatment of diseases involving CD16, like autoimmune diseases, inflammatory disorders, allergies and infections, without inducing any adverse effects. In particular, these antibodies and fragments can prevent or treat anti-drug idiopathic thrombocytopenic purpura (ITP), rheumatoid arthritis (RA) and autoimmune hemolytic anemia (ANA).