A population of early-stage burst-forming unit-eryhtoid (BFU-E) cells characterized by low expression of the Type III Transforming Growth Factor Receptor (TGFRPIII) and uses thereof for producing red blood cells in vitro, genotoxicity analysis of chemicals, drug sensitivity assessment, and drug development. Also described herein are methods for producing the population of early-stage BFU-E cells and methods for producing red blood cells.

A method for producing hematopoietic stem cells and/or hematopoietic progenitor cells from pluripotent stem cells is described. The method includes a step of culturing pluripotent stem cells in the presence of IGF2. A method is described for selecting an induced pluripotent stem cell(s) having high capacity to differentiate into hematopoietic stem cells and/or hematopoietic progenitor cells, or into blood cells, based on the expression level(s) of one or more genes such as TRIM58, CTSF, FAM19A5, and TCERG1L genes, or on the DNA methylation state(s) of the TRIM58, CSMD1, and/or FAM19A5 gene(s).

Modified natural killer (NK) or T cells expressing hematopoietic growth factor receptors are provided. In some embodiments, the NK cells or T cells express a thrombopoietin receptor or an erythropoietin receptor. Methods of treating a subject with cancer are also provided, including administering the modified NK cells or T cells to the subject in combination with a thrombopoietin receptor agonist or erythropoietin receptor agonist, and in some example, interleukin-2, particularly reduced or low-dose amounts of IL-2.

Disclosed herein, are recombinant polypeptides comprising one or more homologous amino acid repeats; and, non-immunogenic bioconjugates comprising recombinant polypeptides comprising one or more homologous amino acid repeats and one or more therapeutic agents. Also, disclosed herein are pharmaceutical compositions including the recombinant polypeptides; and methods of administering the recombinant polypeptides to patients for the treatment of cancer or infections.

Methods for generating enucleated erythroid cells using pluripotent stem cells are provided. The methods permit the production of large numbers of cells. The cells obtained by the methods disclosed may be used for a variety of research, clinical, and therapeutic applications. Methods for generating megakaryocyte and platelets are also provided.

Novel MSC stem-cell culture and therapy methods and culture medium compositions for the purpose of inducing, activating, or priming discrete uniform cell phenotypes to selectively promote or suppress inflammation and immunity, yielding polarized, primed, activated, or induced cells used in cell-based therapy.

Hematopoeitic stem/progenitor cells (HSPC) and/or non-T effector cells are modified to express an extracellular component including a tag cassette. The tag cassette can be used to activate, promote proliferation of, detect, enrich, isolate, track, deplete and/or eliminate modified cells. The cells can also be modified to express a binding domain.

Methods for using cyclin-dependent kinase (CDK) inhibitors to enhance growth and self-renewal of progenitor cells, in vitro and in vivo.

The invention provides culture platforms, cell media, and methods of differentiating pluripotent cells into hematopoietic cells. The invention further provides pluripotent stem cell-derived hematopoietic cells generated using the culture platforms and methods disclosed herein, which enable feed-free, monolayer culturing and in the absence of EB formation. Specifically, pluripotent stem cell-derived hematopoietic cell of this invention include, and not limited to, iHSC, definitive hemogenic endothelium, hematopoietic multipotent progenitors, T cell progenitors, NK cell progenitors, T cells, NK cells, NKT cells and B cells.

The present invention relates to the medical field, in particular to gene editing as a therapeutic approach for the treatment of metabolic diseases affecting the erythroid lineage in a mammalian subject. In invention particular embodiment it refers to the combination of cell reprograming and gene editing for PKD correction as a first example of the potential application of these advanced technologies to metabolic diseases affecting the erythroid lineage. In this sense, PKD patient-specific iPSCs were efficiently generated from PB-MNCs (peripheral blood mononuclear cells) by a SeV non-integrative system and efficiently use to treat pyruvate kinase deficiency. The gene editing strategy for PKLR gene correction was also successfully applied directly to hematopoietic progenitors.