There is provided herein a method for expanding human CD4-CD8- regulatory T cells (DN Tregs) from a population of cells comprising DN Tregs, comprising: culturing the population of cells with artificial antigen presenting cells (APCs), preferably the DN Tregs are αβ-TCR-CD56- or alternatively γ8-TCR+.

Methods for generating/expanding populations of immune cells comprising immune cells specific for an Epstein Barr Virus (EBV) lytic antigen are disclosed, the methods comprising stimulating immune cells specific for an EBV lytic antigen by contacting peripheral blood mononuclear cells (PBMCs) with: (i) one or more peptides corresponding to all or part of one or more EBV lytic antigens; or (ii) antigen presenting cells (APCs) presenting one or more peptides corresponding to all or part of one or more EBV lytic antigens. Also disclosed are populations of immune cells comprising immune cells specific for an EBV lytic antigen expanded according to such methods, and uses thereof.

The present invention is based, in part, on the discovery of anti-SIGLEC-9 composition (e.g., monoclonal antibodies and antigen-binding fragments thereof), that regulate myeloid cell inflammatory phenotypes, such as suppressive myeloid cells, monocytes, macrophages, neutrophils, and/or dendritic cells, including polarization, activation, and/or function, and methods of using such anti-SIGLEC-9 compositions for therapeutic, diagnostic, prognostic, and screening purposes.

In one embodiment, the present application discloses a mammalian autologous vaccine or allogeneic vaccine comprising an effective amount of a mammalian induced pluripotent stem cells (iPSCs) obtained by reprogramming of somatic cells from a patient; wherein the autologous vaccine or the allogeneic vaccine expresses a gene selected from the group consisting of ASTE1, BIRC5, CDCA1, CDKN2A, DEPDC1, EGFR, ERBB2, FOXM1, GPC3, HJURP, HSPA8, HSP90B1, IDH1, IDO1, IGF2BP3, IMPS, KIF20A, KIF20B, MELK, MGAT5, NUF2, PMEL, RAS, TAF1B, TOMM34, TTK, TP53, VEGFR1 and VEGFR2; and wherein the autologous vaccine or the allogeneic vaccine induces an immune response from the patient for the treatment of cancer.

Provided herein are methods of activating immune cells. The method includes providing a population of immune cells and contacting the population of immune cells with a first agent and a second agent. The first agent includes an immune cell activator attached to a first binder moiety, and the second agent includes at least one capture oligomer. The at least one capture oligomer is capable of associating with the first binder moiety. Also provided are kits for activating immune 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.

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.

Provided by the disclosure are compositions and methods for modulating differentiation of regulatory T cells. In some embodiments, methods include selectively decreasing IL-23R activity and/or IL-23R expression without significantly decreasing IL-12RP activity and/or IL-12RP expression.

A chimeric antigen receptor (CAR) comprising a polypeptide comprising an extracellular antigen binding domain comprising a first BCMA binding moiety and a second BCMA binding moiety, wherein the first BCMA binding moiety is a first anti-BCMA single domain antibody, and the second BCMA binding moiety is a second anti-BCMA sdAb; and wherein each of the first and second sdAb is a VHH domain.

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.