A bispecific cytotoxic lymphocyte or macrophage-redirecting autoantibody comprising a cytotoxic lymphocyte or macrophage targeting domain and an autoantibody. Methods for producing bispecific cytotoxic lymphocyte or macrophage-redirecting autoantibody comprising a cytotoxic lymphocyte or macrophage targeting domain and an autoantibody. Methods for treating a subject in need thereof comprising administering to the subject an isolated bispecific cytotoxic lymphocyte or macrophage-redirecting autoantibody.

Therapeutic and diagnostic methods are provided, which methods relate to the induction of expression of calreticulin on phagocytic cells. Specifically, the methods relate to macrophage-mediated programmed cell removal (PrCR), the methods comprising increasing PrCR by contacting a phagocytic cell with a toll-like receptor (TLR) agonist; or down-regulating PrCR by contacting a phagocytic cell with an inhibitor of Bruton's tyrosine kinase (BTK). In some embodiments, an activator of TLR signaling or a BTK agonist is provided in combination with CD4 7 blockade.

Intracellular delivery of a genetic construct to immune cells including: obtaining a deterministic mechanoporation (DMP) platform that includes a substrate having a surface and a plurality of capture sites, each said capture site having a boundary shape at the surface adapted and configured to support thereon a cell, and each said capture site having a bottom and including a sub-micron-scale projection extending from the bottom toward the surface of the substrate, wherein said projection is adapted and configured to penetrate a cell membrane and/or wall of the cell, and wherein the substrate has a plurality of aspiration vias situated at the bottom of the capture sites; introducing the cells to the surface in a liquid media; capturing the cells within the capture sites by applying a first hydrodynamic force; applying a second hydrodynamic force on the captured cell and locally rupturing the membrane and/or wall of the cell with the projection, introducing the genetic construct into the cells, and releasing the porated cells from the capture sites. Also disclosed are methods of chimeric antigen receptor (CAR) T cell adoptive immunotherapy and T cell receptor (TCR) therapy.

The invention relates to an artificial antigen-presenting cell (aAPC) comprising at least one immune stimulatory ligand and co-stimulatory ligands comprising or consisting of CD86, CD70 and CD137L, methods of preparing an aAPC and methods of inducing proliferation of an immune cell or expanding a population of immune cells. The invention also relates to methods for inducing an immune response or treating a medical condition in a subject. The invention further relates to methods of identifying an antigenic peptide or method of identifying or detecting the presence of an immune cell that recognizes an antigen.

The invention provides therapeutic humanized anti-HERV-K antibodies, CAR, or a fusion thereof consisting of a hispecific T ceil engager (BiTE) FOR CD3 and CDS, a DNA-encoded BiTE (DBiTE), or an antibody-drug conjugate (ADC). The invention also relates to peptides, proteins, nucleic acids, and cells for use in immunotherapeutic methods. In particular, the invention relates to the immunotherapy of cancer peptides bound to molecules of the MHC, or peptides as such, which can also be targets of antibodies and other binding molecules.

The present disclosure provides compositions and methods related to chimeric antigen receptors (CARs). In particular, the present disclosure provides CAR-based immunotherapeutic compositions that target tumor cells expressing glypican-3 (GPC3) for the treatment and prevention of cancer.

The present invention relates to peptides, proteins, nucleic acids and cells for use in immunotherapeutic methods. In particular, the present invention relates to the immunotherapy of cancer. The present invention furthermore relates to tumor-associated T-cell peptide epitopes, alone or in combination with other tumor-associated peptides that can for example serve as active pharmaceutical ingredients of vaccine compositions that stimulate anti-tumor immune responses, or to stimulate T cells ex vivo and transfer into patients. Peptides bound to molecules of the major histocompatibility complex (MHC), or peptides as such, can also be targets of antibodies, soluble T-cell receptors, and other binding molecules.

The present disclosure provides for methods of improving the efficacy of T cells. In an aspect, the disclosure further provides for methods of enhancing the persistence of T cells for adoptive cell transfer or therapy (ACT). Cytokine sensitivity assays (CSA) and associated methodology capable of predicting the persistence of adoptively infused T Cells are further provided for by way of the instant disclosure. The disclosure also provides for methods of treating cancer in a subject in need thereof as well as T cells populations produced by methods described herein.

The present invention relates to a method for producing natural killer cells using T cells, and more particularly, to a method for producing natural killer cells, which comprises culturing seed cells using CD4 (+) T cells as feeder cells. The method for producing natural killer cells using T cells according to the present invention is a method capable of producing natural killer cells by selectively proliferating only natural killer cells from a small amount of seed cells while maintaining the high killing activity of the natural killer cells. The method of the present invention can produce a large amount of natural killer cells that can be frozen, and thus is useful for commercialization of cell therapeutic agents.

The present invention provides in certain embodiments compositions comprising at least one CD200 inhibitor, and methods of reversing or modulating immune suppression in a patient having a disease or disorder arising from abnormal cell growth, function or behavior, which method comprises administering to a patient in need thereof a CD200 inhibitor composition.