Abstract: Methods for blocking autoreactive T cell-initiated destruction of tissues in a mammal are provided. In one embodiment, the method comprises administering a purified CD24 polypeptide, a fusion protein comprising such polypeptide, or a biologically active fragment of such polypeptide to a mammalian subject who is suspected of having or predisposed to having an autoimmune disease. In another embodiment, anti-CD24 antibody or anti-CD24 Fab fragments are administered to the subject. In another embodiment, the method comprises administering a CD24 antisense molecule, an expression vector encoding a CD24 antisense molecule, CD24 dsRNAi, or an expression vector encoding CD24 dsRNAi to the subject. The present invention also relates to isolated and purified CD24 fusion proteins employed in the present methods and to transgenic mice that express the human CD24 protein on their T cells and/or their vascular endothelial cells but do not express murine heat shock antigen on any cells.

Abstract: The present invention relates to treating a hematologic cancer using a Hypoxia- Inducible Factor (HIF inhibitor). The invention also relates to inducing acute myeloid leukemia remission using the HIF inhibitor. The invention further relates to inhibiting a maintenance or survival function of a cancer stem cell (CSC) using the HIF inhibitor.

Abstract: The present technology provides methods and compositions for the treatment of tissue-damage related immune dysregulation by administering a composition comprising one or more of CD24; CD24 fragments, variants and derivatives, CD24Fc fusion proteins; HMBG1-binding proteins, binding proteins to HMBG1 Box B; antagonists of HMGB1, polyclonal, monoclonal, recombinant, chimeric, humanized scFv antibodies and antibody fragments to HMGB1 or fragments of HMGB1 and antibodies that bind and suppress the activity of HMGB1 Box B; Siglec 10 agonists such as anti-Siglec 10 antibodies; and combinations thereof to a patient.

Abstract: The present technology provides methods and compositions for the treatment of tissue-damage related immune dysregulation by administering a composition comprising one or more of CD24; CD24 fragments, variants and derivatives, CD24Fc fusion proteins; HMBG1-binding proteins, binding proteins to HMBG1 Box B; antagonists of HMGB1, polyclonal, monoclonal, recombinant, chimeric, humanized scFv antibodies and antibody fragments to HMGB1 or fragments of HMGB1 and antibodies that bind and suppress the activity of HMGB1 Box B; Siglec 10 agonists such as anti-Siglec 10 antibodies; and combinations thereof to a patient.

Abstract: Provided herein are methods of treating a cancer in a subject comprising administering a FOXP3 protein, a nucleic acid encoding a FOXP3 protein, or an inducing compound which induces FOXP3 protein expression. Methods of altering a phenotype of a cancer cell or tumor cell, methods of inhibiting growth of such cells, and methods of inducing apoptosis of these cells are also provided herein. These methods comprise contacting the cell with a FOXP3 protein, a nucleic acid encoding a FOXP3 protein, or an inducing compound which induces FOXP3 protein expression. Further provided herein are diagnostic methods, comprising comparing the expression or structure of a FOXP3 protein or FOXP3 gene in a test sample to that of a normal or prior sample. A method of screening a test compound for anti-cancer activity comprising administering to cells the test compound and measuring FOXP3 protein or FOXP3 gene expression is moreover provided herein.

Abstract: The present technology provides methods and compositions for the treatment of tissue-damage related immune dysregulation by administering a composition comprising one or more of CD24; CD24 fragments, variants and derivatives, CD24Fc fusion proteins; HMBG1-binding proteins, binding proteins to HMBG1 Box B; antagonists of HMGB1, polyclonal, monoclonal, recombinant, chimeric, humanized scFv antibodies and antibody fragments to HMGB1 or fragments of HMGB1 and antibodies that bind and suppress the activity of HMGB1 Box B; Siglec 10 agonists such as anti-Siglec 10 antibodies; and combinations thereof to a patient.

Abstract: Methods for blocking autoreactive T cell-initiated destruction of tissues in a mammal are provided. In one embodiment, the methods involve administering an HAS/CD24 polypeptide or fragment thereof. In some embodiments, the polypeptide or fragment is glycosylated.

Abstract: Provided herein are methods of treating a cancer in a subject comprising administering a FOXP3 protein, a nucleic acid encoding a FOXP3 protein, or an inducing compound which induces FOXP3 protein expression. Methods of altering a phenotype of a cancer cell or tumor cell, methods of inhibiting growth of such cells, and methods of inducing apoptosis of these cells are also provided herein. These methods comprise contacting the cell with a FOXP3 protein, a nucleic acid encoding a FOXP3 protein, or an inducing compound which induces FOXP3 protein expression. Further provided herein are diagnostic methods, comprising comparing the expression or structure of a FOXP3 protein or FOXP3 gene in a test sample to that of a normal or prior sample. A method of screening a test compound for anti-cancer activity comprising administering to cells the test compound and measuring FOXP3 protein or FOXP3 gene expression is moreover provided herein.

Abstract: Although results from preclinical studies in animal models have proven the concept for use of anti-CTLA-4 antibodies in cancer immunotherapy, two major obstacles have hindered their successful application for human cancer therapy. First, the lack of in vitro correlates of the anti-tumor effect of the antibodies makes it difficult to screen for the most efficacious antibody by in vitro analysis. Second, significant autoimmune side-effects have been observed In a recent clinical trial. In order to address these two issues, we have generated human CTLA-4 gene knock-in mice and used them to compare a panel of anti-human CTLA-4 antibodies for their ability to induce tumor rejection and autoimmunity. Surprisingly, while all antibodies induced protection against cancer and demonstrated some autoimmune side effects, the antibody that induced the strongest protection also induced the least autoimmune side effects. These results demonstrate that autoimmune disease does not quantitatively correlate with cancer immunity.

Abstract: The present invention relates to a non-human transgenic animal, particularly a knock in mouse, whose genome comprises a heterologous, chimeric CTLA4 gene. The chimeric CTLA4 gene comprises exon 2 of the human CTLA4 gene, exon 1 and exon 4 of the non-human animal, and exon 3 of the CTLA4 gene of the non-human animal, or preferably, exon 3 of the human CTLA4 gene. The invention also relates to methods by which the transgenic mice are used to screen for monoclonal antibodies or other molecules that enhance immunity to tumors and infectious agents by interacting with the human CTLA4 receptor. The transgenic mice of the present invention are also useful for screening for monoclonal antibodies or other molecules that inhibit autoimmunity and transplant rejection.

Abstract: An image data correction apparatus has a motion information acquisition section, a correction section, and a composition section. The motion information acquisition section acquires motion information indicating spatial distribution of the magnitude of motion, in actual space, of a to-be-imaged portion of a subject. Based on the motion information, the correction section performs correction, which is different from correction in a second region, in a first region of image data collected by a scan by magnetic resonance imaging. The composition section composes individual image data of the first region and the second region that are corrected by the correction section.

Abstract: Methods for screening monoclonal antibodies to CTLA4, monoclonal antibodies to human CTLA4, therapeutic compositions containing the same.

Abstract: The present invention relates to a non-human transgenic animal, particularly a knock in mouse, whose genome comprises a heterologous, chimeric CTLA4 gene. The chimeric CTLA4 gene comprises exon 2 of the human CTLA4 gene, exon 1 and exon 4 of the non-human animal, and exon 3 of the CTLA4 gene of the non-human animal, or preferably, exon 3 of the human CTLA4 gene. The invention also relates to methods by which the transgenic mice are used to screen for monoclonal antibodies or other molecules that enhance immunity to tumors and infectious agents by interacting with the human CTLA4 receptor. The transgenic mice of the present invention are also useful for screening for monoclonal antibodies or other molecules that inhibit autoimmunity and transplant rejection.

Abstract: The present invention relates to a non-human transgenic animal, particularly a knock in mouse, whose genome comprises a heterologous, chimeric CTLA4 gene. The chimeric CTLA4 gene comprises exon 2 of the human CTLA4 gene, exon 1 and exon 4 of the non-human animal, and exon 3 of the CTLA4 gene of the non-human animal, or preferably, exon 3 of the human CTLA4 gene. The invention also relates to methods by which the transgenic mice are used to screen for monoclonal antibodies or other molecules that enhance immunity to tumors and infectious agents by interacting with the human CTLA4 receptor. The transgenic mice of the present invention are also useful for screening for monoclonal antibodies or other molecules that inhibit autoimmunity and transplant rejection.

Abstract: Methods for blocking autoreactive T cell-initiated destruction of tissues in a mammal are provided. In one embodiment, the methods involve administering a pharmaceutical composition comprising an agent selected from a fusion protein comprising an HSA/CD24 polypeptide and a fusion protein comprising a biologically active fragment of an HSA/CD24 polypeptide. In some embodiments, the polypeptide or fragment is glycosylated.

Abstract: Methods for blocking autoreactive T cell-initiated destruction of tissues in a mammal are provided. In one embodiment, the methods involve administering an anti-HAS/CD24 antibody.

Abstract: Methods for blocking autoreactive T cell-initiated destruction of tissues in a mammal are provided. In one embodiment, the methods involve administering an HAS/CD24 polypeptide or fragment thereof. In some embodiments, the polypeptide or fragment is glycosylated.

Abstract: Methods of reducing autoreactive T cell-initiated destruction of tissues in a mammal, comprising administering to the mammal a CD24 dsRNAi molecule or a polynucleotide that encodes a CD24 dsRNAi molecule, wherein said molecule or polynucleotide is administered to the mammal by an ex vivo or in vivo procedure.

Abstract: Methods of reducing autoreactive T cell-initiated destruction of tissues in a mammal, comprising: administering to a mammal a CD24 antisense molecule or a polynucleotide coding for the same, wherein the CD24 antisense molecule or polynucleotide is administered to the mammal by an ex vivo or in vivo procedure.

Abstract: The present invention relates to a non-human transgenic animal, particularly a knock in mouse, whose genome comprises a heterologous, chimeric CTLA4 gene. The chimeric CTLA4 gene comprises exon 2 of the human CTLA4 gene, exon 1 and exon 4 of the non-human animal, and exon 3 of the CTLA4 gene of the non-human animal, or preferably, exon 3 of the human CTLA4 gene. The invention also relates to methods by which the transgenic mice are used to screen for monoclonal antibodies or other molecules that enhance immunity to tumors and infectious agents by interacting with the human CTLA4 receptor. The transgenic mice of the present invention are also useful for screening for monoclonal antibodies or other molecules that inhibit autoimmunity and transplant rejection.