Abstract: Methods of identifying subjects at increased risk of cancer, based upon detection of biofilms and/or biofilm-associated microbes within a subject, are disclosed. Therapies designed to prevent formation and/or reduce the size of biofilms in a subject identified to be at increased risk of cancer based upon detection of biofilms and/or biofilm-associated microbes are disclosed. In particular embodiments, the invention provides for identification of a subject at elevated risk of developing or having colorectal cancer and/or a colorectal adenoma, based upon detection of a biofilm and/or biofilm-associated bacteria within the gastrointestinal tract of the subject (optionally, within a biopsy specimen and/or stool sample of such subject). Therapies involving administration of an antibiotic agent and/or a probiotic agent to a subject, to prevent or reduce biofilm formation within the gastrointestinal tract of the subject, optionally provided in combination with additional cancer therapy, are also disclosed.

Abstract: We demonstrate herein that neuritin controls the homeostasis of regulatory T cells in an antigen dependent manner. Based on this discovery, we describe herein the application of neuritin as a therapeutic agent to manipulate antigen specific regulatory T cells in various disease settings is described. Thus manipulation of Treg cells and DCs through neuritin can be used to enhance immunotherapy of autoimmune diseases, cancer and infectious diseases, as well as enhance lymphocyte engraftment in settings of donor lymphocyte infusion, bone marrow transplant, as well as other types of transplants, and adoptive transfer.

Abstract: The invention features compositions and methods for identifying functional anti-tumor T cell responses.

Abstract: The invention generally features compositions and methods for modulating an immune response. In particular embodiments, such compositions and methods modulate regulatory T cell suppressive activity.

Abstract: The present invention relates to compositions and methods for treating cancer by targeting the Activin signaling pathway. In certain embodiments, combining Activin blockade with immunomodulation alters regulatory T (Treg) cell-mediated immune regulation and treats cancer.

Abstract: The present disclosure relates to compositions and methods for modulating wound healing and regeneration. More particularly, the present disclosure relates to immunomodulatory agents that promote wound healing and tissue regeneration, and that may be optionally used in combination with synthetic or biomaterial scaffolds.

Abstract: The present invention relates to novel compositions and methods to produce 3D organ equivalents of the brain (i.e. “mini-brains”). The invention also relates to methods of using human induced pluripotent stem cells, a combination of growth and other soluble factors and gyratory shaking. Cells from healthy or diseased donors or animals can be used to allow testing different genetic backgrounds. The model can be further enhanced by using genetically modified cells, adding micro-glia or their precursors or indicator cells (e.g. with reporter genes or tracers) as well as adding endothelial cells to form a blood-brain-barrier.

Abstract: Methods of identifying subjects at increased risk of cancer, based upon detection of biofilms and/or biofilm-associated microbes within a subject, are disclosed. Therapies designed to prevent formation and/or reduce the size of biofilms in a subject identified to be at increased risk of cancer based upon detection of biofilms and/or biofilm-associated microbes are disclosed. In particular embodiments, the invention provides for identification of a subject at elevated risk of developing or having colorectal cancer and/or a colorectal adenoma, based upon detection of a biofilm and/or biofilm-associated bacteria within the gastrointestinal tract of the subject (optionally, within a biopsy specimen and/or stool sample of such subject). Therapies involving administration of an antibiotic agent and/or a probiotic agent to a subject, to prevent or reduce biofilm formation within the gastrointestinal tract of the subject, optionally provided in combination with additional cancer therapy, are also disclosed.

Abstract: Blockade of immune checkpoints such as cytotoxic T-lymphocyte antigen-4 (CTLA-4) and programmed death-1 (PD-1) shows promise in patients with cancer. Inhibitory antibodies directed at these receptors have been shown to break immune tolerance and promote anti-tumor immunity. These agents work particularly well in patients with a certain category of tumor. Such tumors may be particularly susceptible to treatment because of the multitude of neoantigens which they produce.

Abstract: Combinations of anti-cancer antibodies and inhibitory antibodies to CD223 overcome immune suppression in cancer patients. The inhibitory antibodies may be generated in an animal by injection of fragments of CD223. Antibodies may be monoclonal antibodies or single chain antibodies or humanized antibodies.

Abstract: In some embodiments, marrow-infiltrating lymphocytes (“MILs”) comprising a chimeric antigen receptor (“CAR”) are provided. In some aspects, the embodiments relate to a method for making a recombinant MIL, comprising obtaining bone marrow comprising MILs; and transfecting, transforming, or transducing the MILs with a nucleic acid encoding a chimeric antigen receptor. In some aspects, the embodiments relate to a method for treating a condition in a subject, comprising administering to the subject a MIL comprising a CAR.

Abstract: In some aspects, the embodiments relate to compositions and methods related to chimeric transmembrane proteins. The chimeric transmembrane proteins may comprise the extracellular domain of an inhibitory receptor, and an intracellular signaling domain that can activate an immune response.

Abstract: Yes-associated protein (Yap), a downstream co-activator of the Hippo pathway, is highly expressed in the Treg cell subset, and is critical to maintain its suppressive activity. Originally discovered in Drosophila melanogaster, the Hippo signaling pathway is a major regulator of cellular growth and proliferation in mammals. Loss of Yap expression in Treg cells can lead to superior anti-tumor immune responses, and thus, Yap is an important immunotherapeutic target for cancer.

Abstract: PD-L1 expression by tumor cells prior to treatment correlates highly with response to anti-PD-1 and anti-PD-L1 therapy (e.g., nivolumab (Bristol-Myers Squibb), pembrolizumab (Merck)) and anti-PD-L1 monotherapy (MPDL3280A (Genentech/Roche)). Nonetheless, the majority of patients with PD-LI(+) tumors do not respond to PD-1 pathway blockade. Distinct gene profiles associated with differential response to treatment with an anti-PD-1 antibody in patients with PD-L1+ renal cell carcinoma have been identified. In particular, a strong up-regulation of genes involved in metabolic functions and pathways was found in patients not responding to the therapy. Additionally, a down-regulation of genes involved in cellular migration functions was found in the same group of patients (non-responders). Specific biomarkers can be used to stratify responders from non-responders for PD-1 pathway blocking drugs.

Abstract: The present invention provides a combination therapy which relies on a small molecule immune stimulator—cyclic-di-nucleotide (CDN)—that activates DCs via a recently discovered cytoplasmic receptor known as STING (Stimulator of Interferon Genes) formulated with allogeneic human tumor cell lines engineered to secrete high amounts of GM-CSF. This combination therapy can provide an ideal synergy of multiple tumor associated antigens, DC recruitment and proliferation, coupled with a potent DC activation stimulus.

Abstract: The invention generally features compositions and methods for modulating an immune response. In particular embodiments, such compositions and methods modulate regulatory T cell suppressive activity.

Abstract: The invention generally features compositions and methods for modulating an immune response. In particular embodiments, such compositions and methods modulate regulatory T cell suppressive activity.

Abstract: Methods of identifying subjects at increased risk of cancer, based upon detection of biofilms and/or biofilm-associated microbes within a subject, are disclosed. Therapies designed to prevent formation and/or reduce the size of biofilms in a subject identified to be at increased risk of cancer based upon detection of biofilms and/or biofilm-associated microbes are disclosed. In particular embodiments, the invention provides for identification of a subject at elevated risk of developing or having colorectal cancer and/or a colorectal adenoma, based upon detection of a biofilm and/or biofilm-associated bacteria within the gastrointestinal tract of the subject (optionally, within a biopsy specimen and/or stool sample of such subject). Therapies involving administration of an antibiotic agent and/or a probiotic agent to a subject, to prevent or reduce biofilm formation within the gastrointestinal tract of the subject, optionally provided in combination with additional cancer therapy, are also disclosed.

Abstract: The invention provides immunogenic compositions comprising neoplastic cells expressing a cytokine (GM-CSF) formulated with at least one TLR agonist and methods of using the composition to induce or enhance an immune response.

Abstract: Cancer therapies that combine epigenetic modulating agent(s) with immune modulating agent(s), which were remarkably identified to provide an improved treatment regimen over single agent therapy, are disclosed. In particular embodiments, the invention provides for improved treatment of NSCLC in patients via administration of exemplary immune modulating agents anti-PD-1 antibody or anti-PD-L1 antibody, which were observed to show enhanced activity in combination with the exemplary epigenetic modulating agent 5-deoxyazacytidine. Further, expression markers of responsive neoplastic cells are also disclosed.