The present invention relates to a Leukocyte-specific protein 1 (LSP1)-deficient T cell-based anticancer immunotherapy. According to the present invention, tumor growth, tumor volume and size were reduced by means of LSP1 knockout, and LSP1 deficiency in T cells increases the number, distribution frequency, migration, and invasion of T cells, and increases the production of an anti-tumor cytokine to inhibit tumor growth and enhance tumor-killing ability. Thus, the present invention can be used for T cell-based immunotherapy.

The invention relates to the field of biomedicine, in particular to an enhanced synthetic T-cell receptor and antigen receptor (STAR) targeting CD19 and CD20, a T cell comprising the synthetic T-cell receptor antigen receptor and the use thereof.

Edited cells, e.g., genomically edited cells, with reduced levels of immune rejection and/or improved persistence are described.

Materials and methods for obtaining populations of lymphocytes and administering the population of lymphocytes to a subject are disclosed herein. In particular, disclosed herein are materials and methods for predicting and improving survival based on the absolute number of natural killer cells observed in the subject after transplant.

Chimeric transmembrane immunoreceptors (CAR) which include an extracellular domain that includes IL-13 or a variant thereof that binds interleukin-13R?2 (IL13R?2), a transmembrane region, a costimulatory domain and an intracellular signaling domain are described.

The present disclosure provides distinct therapeutic populations of cells that form a pharmaceutical composition useful in hematopoietic stem/progenitor cell transplant. For example, the present disclosure provides a therapeutic population of cells, comprising an enriched population of hematopoietic stem/progenitor cells, memory T cells, regulatory T cells, and wherein the population of cells is depleted of na?ve conventional ??-T cells. The present disclosure further provides methods of treatment using the therapeutic population of cells. In other embodiments, the present disclosure provides methods of producing a therapeutic population of cells.

Provided herein are methods and materials for treating autoimmune diseases and alloimmune diseases. Specifically, provided are a pharmaceutical composition comprising a therapeutically effective amount of a population of modified human T cells, wherein the human T cells are modified to comprise a nucleic acid sequence that encodes a chimeric antigen receptor (CAR) construct, wherein the CAR construct comprises an antigen binding domain, wherein the antigen binding domain is specific for a ligand expressed on B cells, plasma cells or plasmablasts in human patients suffering from an autoimmune disease or an alloimmune disease; and a method of treating an autoimmune or an alloimmune disease in a human patient, the method comprising: administering a pharmaceutical composition.

Embodiments of the disclosure include methods and compositions for producing NKT cells effective for immunotherapy and also methods and compositions for providing an effective amount of NKT cells to an individual in need of immunotherapy. In specific embodiments, the NKT cells are CD62L+ and have been exposed to one or more costimulatory agents to maintain CD62L expression. The NKT cells may be modified to incorporate a chimeric antigen receptor, in some cases.

Disclosed herein is a genetically-modified cell comprising in its genome a modified human T cell receptor alpha constant region gene, wherein the cell has reduced cell-surface expression of the endogenous T cell receptor. The present disclosure further relates to methods for producing such a genetically-modified cell, and to methods of using such a cell for treating a disease in a subject.

The present disclosure provides methods of modulating regulatory T-cell activity and function.