Compounds, compositions and methods are provided for the inhibition of ENPP1. Aspects of the subject methods include contacting a sample with a cell impermeable ENPP1 inhibitor to inhibit cGAMP hydrolysis activity of ENPP1. Aspects of the methods include administering to a subject in need thereof a therapeutically effective amount of a CAR expressing immune cell in combination with a therapeutically effective amount of a cell impermeable ENPP1 inhibitor to inhibit the hydrolysis of cGAMP.

Embodiments of the disclosure encompass methods for generating or expanding a population of immune cells specific for a virus, comprising stimulating immune cells specific for a virus by culturing peripheral blood mononuclear cells (PBMCs) in cell culture medium comprising human platelet lysate in the presence of: (i) one or more peptides corresponding to all or part of one or more antigens of the virus; or (ii) antigen presenting cells (APCs) presenting one or more peptides corresponding to all or part of one or more antigens of the virus. In particular embodiments, the cell culture medium comprises a particular percentage of human platelet lysate and/or the PBMCs are depleted of CD45RA-positive cells, for example.

The present invention provides monoclonal antibodies that recognize human Nectin4 with high affinity and specificity and inhibit its binding to T cell immunoreceptor with Ig and ITIM domains (TIGIT). The present invention further provides pharmaceutical compositions comprising the antibodies and methods for their use in cancer immunotherapy and in diagnosis.

The present disclosure provides pharmaceutical compositions comprising a live attenuated bacterial strain of Brucella melitensis, in particular a live attenuated bacterial strain of Brucella melitensis is Brucella melitensis 16M vjbR (BmvjbR). Methods of utilizing the live attenuated bacterial strain of Brucella melitensis for treatment of a patient are also provided, including wherein the patient is in need of treatment for cancer, an autoimmune disorder, and/or an inflammatory disorder.

The present invention relates to CCR9 binding domains. In particular, the invention provides chimeric antigen receptors (CARs) comprising such CCR9 binding domains.

Disclosed herein are engineered immune cells that specifically recognizes mesothelin and expresses IL-15 and optionally CCL19. Also disclosed herein are isolated nucleic acid molecules comprising a polynucleotide encoding a chimeric antigen receptor (CAR) comprising an antibody that specifically recognizes mesothelin, and a 4-IBB intracellular region; and a polynucleotide encoding IL-15; and optionally a polynucleotide encoding CCL19, vectors, pharmaceutical compositions comprising the nucleic acid molecules, and methods of using the engineered immune cells.

The present disclosure generally relates to, inter alia, natural killer (NK) cells including memory-like and cytokine-induced memory like (CIML) NK cells, methods of making and using them e.g. in the treatment of cancer, increasing anti-tumor properties of NK cells.

The present application relates to a modified immune effector cell, wherein the functions of a T cell antigen receptor (TCR) and major histocompatibility complexes (MHCI, MHCII) in the modified immune effector cell are inhibited in a T cell, and the modified immune effector cell comprises a chimeric antigen receptor (CAR) targeting IL13R2. The modified immune effector cell of the present application knocks out TCR and HLA-A genes expressed by the cell while recognizing surface antigens of tumor cells, so that multiple effects of improving the anti-tumor effect of CAR-T cells, prolonging the survival time of the cells, and reducing the immune rejection response caused by allogeneic cell therapy are achieved.

Provided are chimeric receptors for engineering cells for adoptive therapy, including T cells, and the genetically engineered cells. In some embodiments, the chimeric receptors, such as chimeric antigen receptors (CARs) are modified in a junction region by one or more amino acid modifications such that peptide fragments of such region exhibit a lower binding affinity for a human leukocyte antigen (HLA) and/or the region exhibits reduced immunogenicity, including following administration to a subject. In some aspects, also provided are methods and compositions for engineering and producing cells expressing such chimeric receptors, compositions containing the cells, and method for their administration to subjects. In some embodiments, features of the chimeric receptors and engineered cells containing the chimeric receptors result in methods that provide for increased or improved activity, efficacy and/or persistence.

The present invention relates to antibodies, binding polypeptides, and scFvs specific for fibroblast activation protein (FAP) capable of cross reacting with canine, mouse, and human FAP.