The present invention relates to a culture method for increasing the content of NK cells. According to the present invention, the growth rate of immune cells including NK cells can be increased not only in cancer patients but also in persons who are genetically susceptible to cancer or elderly people, and an NK cell fraction and cell-killing ability can also be enhanced.

The invention provides Natural Killer (NK) cells that have a reduced or ablated Signal Regulatory Protein Alpha (SIRPα-) function when compared to a NK cell having an unmodified SIRPα-function that effectively kills a population of cancer cells that express CD47.

The present disclosure relates to genetically modified B cells, including memory cells, differentiated to plasmablasts or plasma cells useful for long term in vivo expression of a transgene, such as a specific antibody or other protein therapeutic. Also disclosed are methods of producing the cells and methods of treatment.

This disclosure relates to methods for enriching a first population of cells positive for a target moiety and/or a second population of cells positive for the target moiety from a sample, wherein a level of the target moiety among the first population of cells is relatively lower than the level of the target moiety among the second population of cells. The methods of this disclosure may also be adapted to assays for determining distinct populations of cells positive for a target moiety in a sample, and to assays for optimizing enrichment conditions. Last, this disclosure relates to kits of components that may be used to carry out the methods and assays.

Methods for developing engineered T-cells for immunotherapy that are both non-alloreactive and resistant to immunosuppressive drugs. The present invention relates to methods for modifying T-cells by inactivating both genes encoding target for an immunosuppressive agent and T-cell receptor, in particular genes encoding CD52 and TCR. This method involves the use of specific rare cutting endonucleases, in particular TALE-nucleases (TAL effector endonuclease) and polynucleotides encoding such polypeptides, to precisely target a selection of key genes in T-cells, which are available from donors or from culture of primary cells. The invention opens the way to standard and affordable adoptive immunotherapy strategies for treating cancer and viral infections.

A composition for culturing peripheral blood monocyte-derived regulatory T cells includes at least one antibody selected from the group consisting of anti-CD2, anti-CD3, anti-CD7, anti-CD8, anti-CD28, anti-CD30L, anti-CD40, anti-CD70, anti-CD80, anti-CD83, and anti-CD86; at least one cytokine selected from the group consisting of interleukin-2, interleukin-4, interleukin-7, interleukin-12, interleukin-15, interleukin-34, and TGF-β; and superoxide dismutase. A regulatory T cell culturing method using this composition is also provided. The regulatory T cells according obtained by this method can be utilized for treatment of autoimmune diseases.

The present invention relates generally to immunotherapy. Disclosed herein are methods for obtaining cytolytic differentiated NKG2A.sup.−NKG2C.sup.+ cells with a given KIR specificity and also compositions comprising these cells as well as the use of these cells for therapy. The NK cell expansion methods provided herein also have non-therapeutic uses.

Methods and compositions for delivering a payload at TnMUC1 positive cancer cells. Anti-TnMUC1 CARs and transgene payloads can be engineered into immune cells so that the transgene payload is expressed and delivered at desired times from the immune cell. Such anti-TnMUC1 CAR T-cells with transgene payloads can be combined with the administration of other molecules, e.g., other therapeutics such as anticancer therapies.

Compounds, compositions, and methods for use in inhibiting the E3 enzyme Cbl-b in the ubiquitin proteasome pathway are disclosed. The compounds, compositions, and methods can be used to modulate the immune system, to treat diseases amenable to immune system modulation, and for treatment of cells in vivo, in vitro, or ex vivo.

Embodiments of the disclosure include methods and compositions related to targeting of CD70-expressing cells with NK cells specifically engineered to bind the CD70 antigen. In particular embodiments, NK cells that are manipulated to expressing CD70-targeting engineered receptors, such as CARs, are utilized to target cancers that express CD70. In certain embodiments, vectors that express the CD70-targeting CARs also express particular a suicide gene and/or one or more particular cytokines.