Abstract: Methods and compositions for cancer immunotherapy are provided. The methods involve the use of a chimeric molecule (e.g., fusion protein) comprising a dimeric NKG2D portion and an Fc portion, which binds one or more NKG2D ligands. In some embodiments, the molecule further comprises a drug moiety (e.g., an IL15/Ra moiety). The methods disclosed herein are useful for the treatment of cancer that is associated with abnormal expression of one or more NKG2D ligands.

Abstract: A pharmaceutical composition contains an antibody or a fragment thereof specific for COL6A3 for the treatment of a cancer. A method of treating a cancer includes administering to a subject in need thereof the pharmaceutical composition. A kit includes a container that contains the pharmaceutical composition. A method of producing an antibody or a fragment thereof against a peptide or a WIC/peptide complex. A method for detecting a diseased tissue includes administering to a subject in need thereof an antibody or a fragment thereof conjugated to a radioisotope and detecting a signal from the radioisotope in the subject. A method for treating a diseased tissue includes administering to a subject in need thereof an antibody or a fragment thereof conjugated to a toxin.

Abstract: Provided are methods of clinical treatment of diffuse large B-cell lymphoma (DLBCL) (e.g., previously untreated, high-risk DLBCL) in human subjects using a bispecific antibody which binds to CD3 and CD20 in combination with standard of care regimen of R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone).

Abstract: A pharmaceutical composition contains an antibody or a fragment thereof specific for COL6A3 for the treatment of a cancer. A method of treating a cancer includes administering to a subject in need thereof the pharmaceutical composition. A kit includes a container that contains the pharmaceutical composition. A method of producing an antibody or a fragment thereof against a peptide or a MHC/peptide complex. A method for detecting a diseased tissue includes administering to a subject in need thereof an antibody or a fragment thereof conjugated to a radioisotope and detecting a signal from the radioisotope in the subject. A method for treating a diseased tissue includes administering to a subject in need thereof an antibody or a fragment thereof conjugated to a toxin.

Abstract: Disclosed are methods of making a genetically modified immune cell for modifying a tumor microenvironment (TME) and methods of modifying a tumor microenvironment (TME). In some embodiments, the method can include delivering a first vector to an immune cell, wherein the first vector comprises a nucleic acid encoding a protein that induces T-cell proliferation, promotes persistence and activation of endogenous or adoptively transferred NK or T cells and/or induces production of an interleukin, an interferon, a PD-1 checkpoint binding protein, HMGB1, MyD88, a cytokine or a chemokine. Methods of modulating the suppression of the immune response in a tumor microenvironment, minimizing the proliferation of tumor and suppressive cells, and increasing the efficiency of an anti-cancer therapy, anti-infection therapy, antibacterial therapy, anti-viral therapy, or anti-tumoral therapy are also provided.

Abstract: The invention provides murine, chimeric, and humanized antibodies that specifically bind to GPC3 and conjugates thereof.

Abstract: Methods of treating melanomas refractory to other therapies using tumor infiltrating lymphocytes are disclosed.

Abstract: Provided are methods, agents and kits for use in assessing the effect of treatment on cancer patients. Further provided is a combination therapy for reducing the administered standard of care doses of anti-cancer agents in treated cancer patients.

Abstract: Embodiments concern methods and composition related to anergic T-cells in patients, such as cancer patients.

Abstract: The present disclosure, relates, in general to methods for improving adverse events in subjects receiving treatment with an anti-CD30 antibody drug conjugate, optionally also receiving accompanying chemotherapy. Adverse events include peripheral neuropathy and neutropenia.

Abstract: Provided is a gRNA targeting HPK1 and a method for editing HPK1 gene. The method can knock out the T cell HPK1 gene, enhance the T cell killing activity, increase the Th1 cytokine level of peripheral blood mononuclear cells, and knock out of the T cell HPK1 gene can also down-regulate the expression of PD-1 and TIM3 on the T cell surface and can inhibit the T cell depletion.

Abstract: Markers of acute myeloid leukemia stem cells (AMLSC) are identified. The markers are differentially expressed in comparison with normal counterpart cells, and are useful as diagnostic and therapeutic targets.

Abstract: Markers of acute myeloid leukemia stem cells (AMLSC) are identified. The markers are differentially expressed in comparison with normal counterpart cells, and are useful as diagnostic and therapeutic targets.

Abstract: The present disclosure provides methods of modulating an immune response in an individual. The present disclosure provides methods of treatment. The present disclosure provides methods comprising administering a multimeric polypeptide (synTac) and an immune checkpoint inhibitor to an individual. The present disclosure provides methods comprising administering a multimeric polypeptide (synTac) to an individual who is undergoing treatment with immune checkpoint inhibitor.

Abstract: Described herein are methods comprising administering to a mammalian subject an effective amount of an annexin chimeric fusion protein, wherein the annexin chimeric fusion protein comprises at least one immunogenic antigen, thereby enhancing the antigen specific immune response relative to administration of the immunogenic antigen alone. Methods and kits for treating or preventing recurrence of hyper proliferating diseases, e.g., cancer, are described. A method may comprise priming a mammal by administering to the mammal an effective amount of a chemotherapeutic agent and boosting the mammal by administering to the mammal an effective amount of an annexin chimeric fusion.

Abstract: Markers of acute myeloid leukemia stem cells (AMLSC) are identified. The markers are differentially expressed in comparison with normal counterpart cells, and are useful as diagnostic and therapeutic targets.

Abstract: The present disclosure relates to composition and methodology for using the CD2 receptor to block viral replication, such as HIV-1 infection. In one embodiment, viral target cells such as blood CD4 T cells can be rendered resistant to HIV through stimulation of the CD2 receptor with either an antibody, a ligand, or a small molecule that binds to the CD2 receptor. Pre-stimulation of CD2 can be used to enhance the anti-HIV immunity and used to promote immune response from HIV infection or from an anti-HIV vaccine.

Abstract: The present disclosure relates to proteins that bind to CD83 and uses thereof, for example, in therapy, prophylaxis, diagnosis, or prognosis.

Abstract: Compositions disclosed herein, and methods of use thereof included those for inhibiting or reducing the incidence of cytokine release syndrome or cytokine storm in a subject undergoing CAR T-cell therapy, methods of treating a cancer or tumor, methods of reducing tumor load, methods of reducing the size or growth rate of a cancer or a tumor, and methods of extending of the survival of a subject suffering from a cancer or tumor, wherein the subjects are administered compositions comprising apoptotic cells or apoptotic cell supernatants. Compositions and methods of use thereof may increase the efficacy of a CAR T-cell cancer therapy. Disclosed herein are also compositions and methods of use thereof for decreasing or inhibiting cytokine production in a subject experiencing cytokine release syndrome or cytokine storm. In certain instances compositions may include additional chemotherapeutic or immunomodulatory agents.

Abstract: Inhibition of human epidermal growth factor receptor 2, human epidermal growth factor receptor 3, or of the heterodimerization of these proteins has presently been found to mitigate mechanically-induced lung injury or a lung-stretch injury. Provided are methods for treating a mechanically-induced lung injury or a lung-stretch injury, for increasing lung compliance, moderating alveolar epithelial permeability, or both in a subject having a mechanically-induced lung injury or a lung-stretch injury, for protecting a subject against a decrease in lung compliance, an increase in alveolar epithelial permeability, or both, as a result of a mechanically-induced lung injury or a lung-stretch injury, such methods involving the administration of an inhibitor of human epidermal growth factor receptor 2 (HER2) or human epidermal growth factor receptor 3 (HER3), or an inhibitor of the heterodimerization of HER2/HER3.