Disclosed is a chimeric antigen receptor with improved persistency.

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 invention provides methods of making immune effector cells (for example, T cells, NK cells) that express a chimeric antigen receptor (CAR), and compositions generated by such methods.

The present invention provides improved and/or shortened processes and methods for reprogramming TILs in order to prepare therapeutic populations of TILs with increased therapeutic efficacy. Such reprogrammed TILs find use in therapeutic treatment regimens.

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 a cell resistant to transplantation immune rejection. The cell expresses a first protein recognizing one or more immune effector cells of a host; preferably the cell has the function of inhibiting or killing the immune effector cells of the host. The present invention also relates to a method for preventing or regulating transplantation immune rejection, and a method for preventing or regulating the attack of NK cells on exogenous cells.

The present invention relates to a method for memory B cell-specific differentiation induction and to uses thereof and, more specifically, to an anti-CD3 antibody or ligand in a biological sample obtained from and individual, a method for memory B cell-specific differentiation induction comprising a step of treating an anti-CD28 antibody or ligand, and a method for detection a memory B cell which is specific to a specific antigen by using same.

The present disclosure provides gene edited modified immune cells or precursors thereof (e.g., gene edited modified T cells) comprising an exogenous T cell receptor (TCR) and/or a chimeric antigen receptor (CAR) having specificity for a target antigen, and an insertion and/or deletion in one or more endogenous gene loci, wherein the endogenous gene loci encode regulators of T cell function, thereby resulting in immune cells having enhanced function. Compositions and methods of treatment are also provided. The present invention provides methods of screening for TCR- or CAR-T cells with enhanced immune function (e.g., T cell efficacy, T cell memory, and/or T cell persistence).

Provided herein are novel blocking chimeric antigen receptors (“bCARs”) and immune cells (e.g., effector and regulatory immune cells) that express such bCARs. Such blocking CARs prevent undesired activation of the immune cells, particularly undesired activation of the immune cells against normal tissue in therapeutic applications. Thus, such bCARs advantageously allow for selective immune cell activation only upon interaction with specific target cells (e.g., tumor cell).

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.