Patent classifications
C12N2501/2304
DETECTION OF A DEFECT ON HLA-E RESTRICTED CD8+ T REGULATORY CELLS
The present invention provides a composition comprising dendritic cells loaded with hHsp60sp, which dendritic cells are from a subject and have been fixed with paraformaldehyde (PFA). The subject may suffer from an autoimmune disease. Also provided are a method for preparing the composition; recombinant human cells comprising a heterologous gene encoding a fusion protein of HLA-E and hHsp60sp or B7sp, and expressing the fusion protein on the surface of the cells; a method for determining a percentage of maximum inhibition of testing the function of the HLA-E restricted CD8+ Treg cells from a subject, determining whether HLA-E restricted CD8+ Treg cells freshly isolated from a subject are defective, or determining whether defective HLA-E restricted CD8+ Treg cells from a subject are correctable; and a method for correcting defective HLA-E restricted CD8+ Treg cells, treating type 1 diabetes (T1D), or treating multiple sclerosis (MS).
Generation of HPV-specific T-cells
Embodiments of the disclosure concern methods and compositions for immunotherapy for human papillomavirus infection and diseases associated therewith. In specific embodiments, methods concern production of immune cells that target one or more antigens of HPV16 and/or HPV18, including methods with stimulation steps that employ IL-7 and IL-15, but not IL-6 and/or IL-12. Other specific embodiments utilize stimulations in the presence of certain cells, such as costimulatory cells and certain antigen presenting cells.
IL-23R antagonists to reprogram intratumoral T regulatory cells into effector cells
Provided by the disclosure are compositions and methods for modulating differentiation of regulatory T cells. In some embodiments, methods include selectively decreasing IL-23R activity and/or IL-23R expression without significantly decreasing IL-12RP activity and/or IL-12RP expression.
Indole regulation of antigen presenting cells
The disclosure provides methods and compositions for affecting the development of antigen presenting cell (APC, e.g., a macrophage or dendritic cell). The methods include maturing an APC, promoting anti-inflammatory phenotype, promoting development of a T regulatory cell (Treg) from a naive T cell. The methods generally include exposing an APC to a tryptophan derived microbiota metabolite (TDMM), such as an anti-inflammatory or pro-mucosal TDMM, and permitting the APC to mature. In some embodiments, the conditioned APC is exposed to a naive T cell to further promote development of a T regulatory cell (Treg). In some embodiments, the TDMM is selected from the group consisting of indole, indole-3-acetate, 5-hydroxyindole, and indole-3-pyruvate.
Methods to Enhance Tumor Immunogenicity and Compositions for Autologous Cancer Immunotherapeutic Products Using Modified Tumor Cells and Modified Dendritic Cells
The present specification provides methods for augmenting the antigenic content, especially of tumor-associated antigens (TAA), and immunogenicity of cancer cells; methods for enhancing cross-presentation in dendritic cells, compositions comprising such manipulated cells derived from single cancer patients; and methods of using those compositions as a personal immunotherapeutic product to treat the donor patient's cancer.
B CELLS FOR IN VIVO DELIVERY OF THERAPEUTIC AGENTS
The present disclosure relates to genetically modified B cells, including memory cells, differentiated to plasmablasts or plasma cells useful for long term in vivo expression of a transgene, such as a specific antibody or other protein therapeutic. Also disclosed are methods of producing the cells and methods of treatment.
COMPOSITION FOR CULTURING PERIPHERAL BLOOD MONOCYTE-DERIVED REGULATORY T CELL AND REGULATORY T CELL CULTURING METHOD USING SAME
A composition for culturing peripheral blood monocyte-derived regulatory T cells includes at least one antibody selected from the group consisting of anti-CD2, anti-CD3, anti-CD7, anti-CD8, anti-CD28, anti-CD30L, anti-CD40, anti-CD70, anti-CD80, anti-CD83, and anti-CD86; at least one cytokine selected from the group consisting of interleukin-2, interleukin-4, interleukin-7, interleukin-12, interleukin-15, interleukin-34, and TGF-β; and superoxide dismutase. A regulatory T cell culturing method using this composition is also provided. The regulatory T cells according obtained by this method can be utilized for treatment of autoimmune diseases.
MACROPHAGE-DERIVED ENGINEERED VESICLES FOR TARGETED DELIVERY AND TREATMENT
Compositions and methods described in this document make use of macrophage derived engineered vesicles (MEV) having specificity for delivery to a target environment, for use in modifying macrophage phenotype and/or treating a condition. Further disclosed are MEV derived from a specific phenotype encapsulating a therapeutic agent for targeted therapeutic delivery.
METHODS OF B CELL EXPANSION FOR USE IN CELL THERAPY
The invention disclosed herein relates to improved methods for expanding cell populations, particularly B cell populations. The invention further relates to improved B-cell expansion media, compositions comprising expanded B cells and methods of using such expanded B cells. The invention further relates to methods of treating diseases or disorders wherein a population of B cells is obtained and cultured, and wherein said B cells are engineered to express a payload and/or a chimeric receptor, and wherein said B cells are administered to a subject.
NOVEL METHOD
There is provided inter alia according to the invention an ex vivo method of obtaining tolerogenic antigen presenting cells (APCs) that have the capability to induce tolerance in the immune system to an antigen, the method comprising (a) isolating monocytes from a sample obtained from a mammal; and (b) culturing the isolated monocytes in a cell culture to induce differentiation of the monocytes into antigen presenting cells having a tolerogenic phenotype, wherein the cell culture comprises (i) retinoic acid and TGFbeta, (ii) retinoic acid, TGFbeta and an AhR agonist or (iii) retinoic acid and an AhR agonist.