The present disclosure relates to genetically modified T cells comprising a transgene encoding an engineered antigen specific receptor, wherein expression of an endogenous gene selected from MNK1, MNK2, or both are inhibited in the genetically modified T cell in order to enhance central memory T cell subsets in cellular immunotherapy compositions.

The present invention relates to a novel chimeric antigen receptor and to a pharmaceutical composition for preventing or treating containing the same.

Embodiments of the disclosure concern compositions and methods of use related to particular immortalized cells, including cardiac stem cells, obtained from a pediatric or neonatal individual. In specific embodiments, the immortalized cells, or conditioned medium from the cells, or partial or total secretomes thereof, are provided in an effective amount to an individual in need thereof either alone or in combination with cardiac stem cells.

The present invention aims to solve a problem in T-cell transfer therapy and the like, which is T-cell exhaustion, and to provide a technique to enhance T cell activity. T cells having cell surface markers of CD45RA.sup.+ and CCR7.sup.+ can be produced by culturing activated T cells in the presence of (a) a conditioned medium derived from stromal cells or (b) CXCL12.

Provided herein are recombinant nucleic acids encoding T cell receptor (TCR) fusion proteins (TFPs), modified human immune cells expressing the encoded molecules, and methods of use thereof for the treatment of diseases, including cancer.

Provided herein are novel blocking chimeric antigen receptors (“bCARs”) and immune cells (e.g., effector and regulatory immune cells) that express such bCARs. Such blocking CARs prevent undesired activation of the immune cells, particularly undesired activation of the immune cells against normal tissue in therapeutic applications. Thus, such bCARs advantageously allow for selective immune cell activation only upon interaction with specific target cells (e.g., tumor cell).

The present invention provides a nucleic acid construct comprising the following structure: A-X-B in which A is nucleic acid sequence encoding a first polypeptide which comprises a first signal peptide; B is nucleic acid sequence encoding a second polypeptide which comprises a second signal peptide and X is a nucleic acid sequence which encodes a cleavage site, wherein the first signal peptide or the second signal peptide comprises one or more mutation(s) such that it has fewer hydrophobic amino acids.

Disclosed are antibodies against MUC1, MUC1-CAR compositions and methods for use of these antibodies and compositions to target a MUC1 protein, wherein a cell expressing the MUC1 protein may be targeted and killed by, for instance, a cytotoxic T cell.

A method is disclosed for separating cells from a lung. Mechanical pressure can be used in one stage of the process to increase the yield of separated cells, including alveolar type II cells.

The present disclosure features, at least in part, methods for conserving cell function, e.g., immune cell function, e.g., after one or more cycles of freezing and/or thawing the nucleated cell. In embodiments, the methods comprise contacting an immune cell with a protein nanoparticle comprising an IL-15 complex.