Systems and methods to selectively protect therapeutic cells by reducing CD33 expression in the therapeutic cells using base editors and targeting non-therapeutic cells with an anti-CD33 therapy are described. The selective protection results in the enrichment of the therapeutic cells while simultaneously targeting any diseased, malignant and/or non-therapeutic CD33 expressing cells within a subject.

The invention relates to: a composition for culturing natural killer cells, comprising, as an active ingredient, a fusion protein comprising an IL-2 protein and a CD80 protein; and a method for preparing natural killer cells by using same. Particularly, a composition for culturing natural killer cells, comprising, as an active ingredient, a fusion protein comprising IL-2 or a variant thereof and CD80 or a fragment thereof, of the present invention; promotes the proliferation of natural killer cells, induces the expression of CD16 and NKp46, and increases the expression and secretion of granzyme B and perforin, thereby being effectively usable in the preparation of natural killer cells having an excellent anticancer immune function.

The present invention relates to methods for developing engineered T-cells for immunotherapy and more specifically to methods for modifying T-cells by inactivating at immune checkpoint genes, preferably at least two selected from different pathways, to increase T-cell immune activity 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 highly efficient adoptive immunotherapy strategies for treating cancer and viral infections.

The present invention relates to Chimeric Antigen Receptors (CAR) that are recombinant chimeric proteins able to redirect immune cell specificity and reactivity toward selected membrane antigens, and more particularly in which extracellular ligand binding is a scFV derived from a BCMA monoclonal antibody, conferring specific immunity against BCMA positive cells. The engineered immune cells endowed with such CARs are particularly suited for treating lymphomas, multiple myeloma and leukemia.

Provided herein are methods for ex vivo expansion of a T cells, including tumor-reactive T cells, and compositions containing such T cells. Also provided are methods for treating diseases and conditions such as cancer using compositions of the present disclosure.

The present invention provides a human CD16.sup.+ natural killer cell line and a CAR-expressing human CD16.sup.+ natural killer cell line. These human CD16.sup.+ natural killer cell line and a CAR-expressing human CD16.sup.+ natural killer cell line does not include synthetic, genetically modified or purposely deliberately delivered polynucleotide encoding the CD16 receptor and are non-tumorigenic cell lines. Therefore, this human CD16.sup.+ natural killer cell line and a CAR-expressing human CD16.sup.+ natural killer cell line might provide considerable long-term safety for disease treatment.

The present invention relates to a method for culturing natural killer cells (NK cells) applied to immune therapy and, more particularly, to a medium addition kin for culturing NK cells with which lymphocytes derived from human peripheral blood can be cultured to effectively amplify and activate NK cells, which have an outstanding therapeutic effect on malignant tumors, while remarkably increasing the share of NK cells, and an NK cell culturing method using the kit.

[Problem] To provide a cell preparation including mesenchymal stem cells (MSCs) having a high therapeutic effect. [Solution] A method for producing activated mesenchymal stem cells, including a step of culturing MSCs in a medium containing an activator that includes an extract from a mammalian fetal appendage as an active ingredient, using a cell culture carrier having a three-dimensional structure formed of a fiber is provided. A marker for a therapeutic effect of MSCs selected from the group consisting of p16.sup.ink4a, p14.sup.ARF, CDK4, CDK6, RB, and CD47, a method for determining a therapeutic effect using the marker, a method for determining suitability of MSCs to be treated with a treatment for enhancing a therapeutic effect of MSCs, a cell preparation including MSCs, and a method for producing the same are also provided.

The present disclosure relates in some aspects to methods, cells, and compositions for preparing cells and compositions for genetic engineering and cell therapy. Provided in some embodiments are streamlined cell preparation methods, e.g., for isolation, processing, incubation, and genetic engineering of cells and populations of cells. Also provided are cells and compositions produced by the methods and methods of their use. The cells can include immune cells, such as T cells, and generally include a plurality of isolated T cell populations or types. In some aspects, the methods arc capable of preparing of a plurality of different cell populations for adoptive therapy using fewer steps and/or resources and/or reduced handling compared with other methods.

The invention pertains to the field of adaptive cell immunotherapy. It aims at reducing the occurrence of translocations and cell deaths when several specific endonuclease reagents are used altogether to genetically modify primary immune cells at different genetic loci. The method of the invention allows to yield safer immune primary cells harboring several genetic modifications, such as triple or quadruple gene inactivated cells, from populations or sub-populations of cells originating from a single donor or patient, for their subsequent use in therapeutic treatments.