摘要:
A method of altering the specific, systemic immune response of an individual to a target antigen by the co-administration of a cytokine an adhesion or accessory molecule and the target antigen. The target antigen may be a tumor cell, a tumor cell antigen, an infectious agent or other foreign antigen, or other antigens to which an enhanced systemic immune response is desirable. Alternatively, the antigen may be a non-foreign antigen when a suppression of a systemic immune response is desired. The resulting systemic immune response is specific for the target antigen.
摘要:
A method of altering the specific, systemic immune response of an individual to a target antigen by the co-administration of a cytokine an adhesion or accessory molecule and the target antigen. The target antigen may be a tumor cell, a tumor cell antigen, an infectious agent or other foreign antigen, or other antigens to which an enhanced systemic immune response is desirable. Alternatively, the antigen may be a non-foreign antigen when a suppression of a systemic immune response is desired. The resulting systemic immune response is specific for the target antigen.
摘要:
Described are uses of an agent that reduces B7-H1 interaction with PD-1, and particularly monoclonal antibodies that bind to B7-H1 and interfere with B7-H1 interaction with PD-1 in combination with a vaccine to provide synergistic effects. The application provides methods of treatment and vaccination based on the combination of these compounds on T cell responses.
摘要:
The present invention relates to methods for modulating, i.e., agonizing or antagonizing, Stat3 (Signal Transducer and Activator of Transcription3) signaling activity for use in gene therapy. Inhibition and/or activation of Stat3 signaling is an effective approach to modulate angiogenesis and the immune response for treatment and/or prevention of inflammation, infection, inflammation, immune disorders, and ischemia.
摘要:
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.
摘要:
To increase the effective affinity of soluble analogs of peptide/MHC molecules for their cognate ligands, divalent peptide/MHC complexes were constructed. Using a recombinant DNA strategy, DNA encoding the MHC class I was ligated to DNA coding for murine Ig heavy chain. MHC/Ig complexes were exploited to homogeneously load with peptides of interest. The results of flow cytometry demonstrated that the pepMHC/Ig complexes bound specifically with high affinity to cells bearing their cognate receptors. pepMHC/Ig complexes are also useful in modulating effector functions of antigen-specific T cells. These pepMHC/Ig complexes are useful for studying TCR/MHC interactions and lymphocyte tracking and have uses as specific regulators of immune responses.
摘要:
Regulatory T cells (Treg) limit autoimmunity but can also attenuate the magnitude of anti-pathogen and anti-tumor immunity. Understanding the mechanism of Treg function and therapeutic manipulation of Treg in vivo requires identification of Treg selective receptors. A comparative analysis of gene expression arrays from antigen specific CD4+ T cells differentiating to either an effector/memory or a regulatory phenotype revealed Treg selective expression of LAG-3 (CD223), a CD4-related molecule that binds MHC class II. LAG-3 expression on CD4+ T cells correlates with the cells' in vitro suppressor activity, and ectopic expression of LAG-3 on CD4 T cells confers suppressor activity on the T cells. Antibodies to LAG-3 inhibit suppression both in vitro and in vivo. LAG-3 marks regulatory T cell populations and contributes to their suppressor activity.
摘要:
The invention provides methods and compositions for targeting a separately generated immune response to a specific organ or tissue, e.g. one affected by cancer, using one or more agents with a tropism for the organ or tissue or that can be specifically localized to the desired organ or tissue. For example, the invention provides methods ands compositions for treating liver metastases from colorectal cancer using a combination of a granulocyte/macrophage colony stimulating factor (GM-CSF) augmented tumor cell vaccination and Listeria monocytogenes (LM) infection.
摘要:
To increase the effective affinity of soluble analogs of peptide/MHC molecules for their cognate ligands, divalent peptide/MHC complexes were constructed. Using a recombinant DNA strategy, DNA encoding the MHC class I was ligated to DNA coding for murine Ig heavy chain. MHC/Ig complexes were exploited to homogeneously load with peptides of interest. The results of flow cytometry demonstrated that the pepMHC/Ig complexes bound specifically with high affinity to cells bearing their cognate receptors. pepMHC/Ig complexes are also useful in modulating effector functions of antigen-specific T cells. These pepMHC/Ig complexes are useful for studying TCR/MHC interactions and lymphocyte tracking and have uses as specific regulators of immune responses.
摘要:
The present invention relates to methods for treating and/or preventing cancer. In particular the present invention relates to ex vivo immunotherapeutic methods. The methods comprise decreasing Stat3 (signal transducer and activator of transcirption3) expression and/or function in tumor cells and the administration of such cells to a subject in need of treatment and/or prevention. Other methods of the invention comprise activation T-cells by co-culturing the T-cells with the tumor cells with decreased Stat3 expression or function. The invention further encompasses methods comprising decreasing Stat3 expression or function in antigen-presenting cells and co-administering tumor cells and the antigen-presenting cells with decreased Stat3 function to a patient. The invention further relates to methods for stimulating dendritic cell differentiation.