The disclosure concerns a method for cancer treatment by in vivo priming and activation of natural killer cells for achieving tumor cell lysis. The method includes introducing into a patient a priming tumor cell preparation (PTCP) derived from a first tumor cell line, which is irradiated to inactivate the first tumor cells or a membrane preparation thereof, the first tumor cells having known priming ligands on the membrane surface thereof. The patient's rest NK cells are contacted by the PTCP in vivo, resulting in primed NK cells, which are characterized by upregulation of CD69, shedding of CD16, or a combination of CD69+ and CD16. These primed NK cells then contact second tumor cells, the cancer, and are configured to lyse and kill the second tumor cells.

The present invention provides, in certain aspects, a natural killer (NK) cell that expresses all or a functional portion of interleukin-15 (IL-15), and methods for producing such cells. The invention further provides methods of using a natural killer (NK) cell that expresses all or a functional portion of interleukin-15 (IL-15) to treat cancer in a subject or to enhance expansion and/or survival of NK cells.

The present invention relates to expanded NK cells. The NK cells have been expanded ex vivo, are activated and have a cytotoxic phenotype. The cytotoxicity against malignant cells is markedly increased compared to non-expanded NK cells. The invention also relates to a method of treatment.

The invention provides a method of determining T cell function in a subject in need of immunotherapy comprising: i) providing a blood sample comprising a population of T cells from the subject; ii) activating the T cells in the sample; and iii) assaying an expression level of one or more T cell activation markers using quantitative real time PCR (qPCR) after activating the T cells in the sample.

The present invention relates to a method for culturing natural killer cells, using genetically modified T cells. A method for culturing natural killer cells, using genetically modified T cells according to the present invention enables the effective proliferation and production of natural killer cells from a smaller amount of source cells. In addition, the method enhances the cytolytic activity of natural killer cells. Therefore, the method for culturing natural killer cells, using genetically modified T cells according to the present invention can find useful applications in commercializing cell therapy products. Further, the natural killer cells produced by the culturing method of the present invention can be useful as a cell therapy product.

The present invention provides, in certain aspects, a natural killer (NK) cell that expresses all or a functional portion of interleukin-15 (IL-15), and methods for producing such cells. The invention further provides methods of using a natural killer (NK) cell that expresses all or a functional portion of interleukin-15 (IL-15) to treat cancer in a subject or to enhance expansion and/or survival of NK cells.

This disclosure relates to compositions and methods for treating cancer using armored chimeric antigen receptor cells.

The present disclosure provides compositions and methods comprising recombinant particles suitable for specifically delivering one or more chimeric antigen receptors to immune effector cells in vivo.

The present disclosure provides compositions and methods comprising recombinant particles suitable for specifically delivering one or more chimeric antigen receptors to immune effector cells in vivo.

Current invention relates to a polynucleotide encoding activating chimeric receptors comprising engineered Natural Killer Group 2 member C (NKG2C) having enhanced affinity for HLA class I histocompatibility antigen alpha chain E (HLA-E)/peptide complex or an extracellular receptor domain of NKG2A coupled to an effector domain. It also relates to NK cells expressing such constructs and the use of these NK cells to induce cytotoxicity. It further exemplifies that the NK cells expressing polynucleotide encoding NKG2C (SIIS)/CD94/DAP12 or NKG2C/CD94/4-1 BB/CD3z showed enhanced NK cytotoxicity against cancer cells.