Patent application number | Description | Published |
20090311694 | Splice variants of human IL-23 receptor (IL-23R) mRNA and use of a delta 9 isoform in predicting inflammatory bowel diseases - There is disclosed the cloning and identification of human IL-23R splice variants caused by alternative splicing of the IL-23R mRNA in human. Alternative mRNA forms occur through skipping one, multiple full exons or partial exons, within the IL-23R gene. A total of twenty-five (25) different IL-23R transcripts were identified. A novel exon deletion (exon 9) isoform in the interleukin 23 receptor is disclosed, denoted as Δ9. The present application also describes a quantitative assay to measure different IL-23R isoform. Detection of Δ9 isoform of IL-23R is predominantly present in colon and cervical tissues. A decrease in Δ9 is observed in inflamed colon tissues in Crohn's patients. There is disclosed a method of predicting Crohn's disease by measuring Δ9 isoform of IL-23R. | 12-17-2009 |
20110237643 | Identification of a Novel repressor on IFN-lambda promoter and siRNA against ZEB1 and BLIMP-1 to increase IFN-lambda gene activity - The present invention is directed to the identification of a novel repressor located between ˜1.2 kb to ˜1.6 kb from the translation start site of the IFN-λ1 promoter. The present invention provides a method of using siRNAs against ZEB1 (binds to the repressor region) and BLIMP-1 (binds outside the repressor region) and increases the promoter activity of IFN-λ1 (i.e., increases the production of IFN-λ1 protein). siRNAs against ZEB1 mRNA or BLIMP-1 mRNA increase IFN-λ1 gene activity. There is provided a therapeutic application of siRNAs against ZEB1 and BLIMP-1 mRNAs in treating a mammal (including a human) by increasing the production of IFN-λ1 protein that promotes an anti-viral response as well as treats asthma diseases. | 09-29-2011 |
20110268707 | Ex-vivo treatment of peripheral blood leukocytes with IFN-lambda - The present invention provides an ex vivo method of treating plasmacytoid dendritic cells (pDC) in Th2- or Th17-associated diseases by modulating the cytokine expression or secretion using interferon lambda (IFN-λ). For the Th-2 or Th17-associated diseases, pDC cells from a patient having the disease are exposed ex vivo with IFN-λ in an effective amount to inhibit cytokine releases. The IFN-λ exposed pDC are administered back into the patient. The present invention also provides a method of ex vivo IFN-λ treatment of pDC, in conjunction with co-administration of a composition comprising IFN-λ. | 11-03-2011 |
20120058081 | Ex-vivo treatment of peripheral blood leukocytes with IFN-lambda - The present invention provides a method of treating Th2-associated diseases and disorders by modulating the expression or secretion of IL-4, IL-5 and IL-13 using interferon lambda (IFN-λ). For Th2-associated diseases and disorders, cells of a patient having a Th2-associated disease or disorder are treated ex vivo, with IFN-λ and returned to the patient. The present invention also provides a method of ex vivo treatment, in conjunction with co-administration of IFN-λ | 03-08-2012 |
20120071422 | Therapeutic application of isolated naturally-occuring soluble truncated forms of IL-23 receptor - The present invention relates to an isolated naturally-occurring soluble truncated IL-23Rα protein, which is a translated protein resulting from a mRNA splice variant of IL-23Rα. The soluble IL-23Rα proteins (e.g., Δ9 and Δ8,9) represents a novel soluble IL-23Rα protein, which is lacking a transmembrane domain and has a unique eight (8) amino acids (GLKEGSYC) at its C-terminus end (due to frame-shift). ELISA reveals that Δ9 is present in blood and can serve as a diagnostic tool for auto-immune diseases including Crohn's disease. There is also provided a method of recombinant production for this soluble truncated form of IL-23Rα protein. More importantly, the present invention provides an utility application of the Δ9 and Δ8,9 protein in inhibit IL-23R-mediated cell signaling. More particularly, Δ9 and Δ8,9 blocks STAT3 formation as well as Th17 maturation. There is provided a therapeutic application of Δ9 and Δ8,9 in treating a human patient inflicted with Crohn's disease. | 03-22-2012 |
20120171704 | Elisa for a naturally-occurring soluble truncated form of IL-23 receptor - A naturally-occurring soluble truncated IL-23Rα protein (i.e., Δ9 IL-23Rα) is shown to be present in a biological sample and can serve as a diagnostic tool for autoimmune diseases. There is provided an enzyme-linked immunosorbent assay (ELISA) and test kit for the serological detection of the soluble truncated form of IL-23Rα protein. More particularly, antibody-sandwich ELISA method and kits for Δ9 IL-23Rα as an antigen were developed to detect Δ9 IL-23Rα levels in biological samples from a mammal and a human patient and are used as a diagnostic index. The present disclosed ELISA has utility as a diagnostic tool to detect Crohn's disease in patients using EDTA-plasma. | 07-05-2012 |
20120244542 | SPLICE VARIANTS OF HUMAN IL-23 RECEPTOR (IL-23R) mRNA AND USE OF A DELTA9 ISOFORM IN PREDICTING INFLAMMATORY BOWEL DISEASES - There is disclosed the cloning and identification of human IL-23R splice variants caused by alternative splicing of the IL-23R mRNA in human. Alternative mRNA forms occur through skipping one, multiple full exons or partial exons, within the IL-23R gene. A total of twenty-five (25) different IL-23R transcripts were identified. A novel exon deletion (exon 9) isoform in the interleukin 23 receptor is disclosed, denoted as Δ9. The present application also describes a quantitative assay to measure different IL-23R isoform. Detection of Δ9 isoform of IL-23R is predominantly present in colon and cervical tissues. A decrease in Δ9 is observed in inflamed colon tissues in Crohn's patients. There is disclosed a method of predicting Crohn's disease by measuring Δ9 isoform of IL-23R. | 09-27-2012 |
20120245325 | SPLICE VARIANTS OF HUMAN IL-23 RECEPTOR (IL-23R) mRNA AND USE OF A DELTA9 ISOFORM IN PREDICTING INFLAMMATORY BOWEL DISEASES - There is disclosed the cloning and identification of human IL-23R splice variants caused by alternative splicing of the IL-23R mRNA in human. Alternative mRNA forms occur through skipping one, multiple full exons or partial exons, within the IL-23R gene. A total of twenty-five (25) different IL-23R transcripts were identified. A novel exon deletion (exon 9) isoform in the interleukin 23 receptor is disclosed, denoted as Δ9. The present application also describes a quantitative assay to measure different IL-23R isoform. Detection of Δ9 isoform of IL-23R is predominantly present in colon and cervical tissues. A decrease in Δ9 is observed in inflamed colon tissues in Crohn's patients. There is disclosed a method of predicting Crohn's disease by measuring Δ9 isoform of IL-23R. | 09-27-2012 |
20130029907 | Novel Polypeptides That Bound to IL-23 Receptor and Inhibit Binding of IL-23 and Cell Signaling Thereof - The present invention relates to novel polypeptides that bind to IL-23 receptor and inhibit the binding of IL-23 to its corresponding receptor and cell signaling thereof. The novel polypeptides of the present invention has a core structure of WX | 01-31-2013 |
20130035365 | Anti-sense oligonucleotides targeted against exon 9 of IL-23R alpha gene and method of using same to induce exon skipping and to treat inflammatory bowel diseases - The present invention relates to anti-sense oligonucleotides (AONs) used to induce exon 9 skipping in IL-23Rα gene. Exon 9 skipping of the IL23Rα gene ultimately causes specific induction of a novel soluble truncated IL-23Rα (Δ9) protein, characterized by a lack in a transmembrane domain and has a unique eight (8) amino acids (GLKEGSYC) at its C-terminus end as a result of frame-shift. The present invention provides a utility application of the use of AONs to induce production of a Δ9 protein which inhibits IL-23R-mediated cell signaling. More particularly, Δ9 protein blocks STAT3 formation as well as Th17 maturation. There is provided a therapeutic application of AONs in treating a mammal such as a human patient inflicted with Crohn's disease. | 02-07-2013 |
20130172272 | Novel Polypeptides That Bound to IL-23 Receptor and Inhibit Binding of IL-23 and Cell Signaling Thereof - The present invention relates to novel polypeptides that bind to IL-23 receptor and inhibit the binding of IL-23 to its corresponding receptor and cell signaling thereof. The novel polypeptides of the present invention has a core structure of WX | 07-04-2013 |
20130183755 | THERAPEUTIC APPLICATION OF ISOLATED NATURALLY-OCCURRING SOLUBLE TRUNCATED FORMS OF IL-23 RECEPTOR - The present invention relates to an isolated naturally-occurring soluble truncated IL-23Rα protein, which is a translated protein resulting from a mRNA splice variant of IL-23Rα. The soluble IL-23Rα proteins (e.g., Δ9 and Δ8,9) represents a novel soluble IL-23Rα protein, which is lacking a transmembrane domain and has a unique eight (8) amino acids (GLKEGSYC) at its C-terminus end (due to frame-shift). ELISA reveals that Δ9 is present in blood and can serve as a diagnostic tool for auto-immune diseases including Crohn's disease. There is also provided a method of recombinant production for this soluble truncated form of IL-23Rα protein. More importantly, the present invention provides an utility application of the Δ9 and Δ8,9 protein in inhibit IL-23R-mediated cell signaling. More particularly, Δ9 and Δ8,9 blocks STAT3 formation as well as Th17 maturation. There is provided a therapeutic application of Δ9 and Δ8,9 in treating a human patient inflicted with Crohn's disease. | 07-18-2013 |
20130196333 | SPLICE VARIANTS OF HUMAN IL-23 RECEPTOR (IL-23R) mRNA AND USE OF A DELTA 9 ISOFORM IN PREDICTING INFLAMMATORY BOWEL DISEASES - There is disclosed the cloning and identification of human IL-23R splice variants caused by alternative splicing of the IL-23R mRNA in human. Alternative mRNA forms occur through skipping one, multiple full exons or partial exons, within the IL-23R gene. A total of twenty-five (25) different IL-23R transcripts were identified. A novel exon deletion (exon 9) isoform in the interleukin 23 receptor is disclosed, denoted as Δ9. The present application also describes a quantitative assay to measure different IL-23R isoform. Detection of Δ9 isoform of IL-23R is predominantly present in colon and cervical tissues. A decrease in Δ9 is observed in inflamed colon tissues in Crohn's patients. There is disclosed a method of predicting Crohn's disease by measuring Δ9 isoform of IL-23R. | 08-01-2013 |
20130338211 | NOVEL REPRESSOR ON IFN-LAMBDA PROMOTER AND SIRNA AGAINST ZEB1 AND BLIMP-1 TO INCREASE IFN-LAMBDA GENE ACTIVITY - The present invention is directed to the identification of a novel repressor located between ˜1.2 kb to ˜1.6 kb from the translation start site of the IFN-λ1 promoter. The present invention provides a method of using siRNAs against ZEB1 (binds to the repressor region) and BLIMP-1 (binds outside the repressor region) and increases the promoter activity of IFN-λ1 (i.e., increases the production of IFN-λ1 protein). siRNAs against ZEB1 mRNA or BLIMP-1 mRNA increase IFN-λ1 gene activity. There is provided a therapeutic application of siRNAs against ZEB1 and BLIMP-1 mRNAs in treating a mammal (including a human) by increasing the production of IFN-λ1 protein that promotes an anti-viral response as well as treats asthma diseases. | 12-19-2013 |
20140050700 | EX-VIVO TREATMENT OF PERIPHERAL BLOOD LEUKOCYTES WITH IFN-Lambda - The present invention provides a method of treating Th2-associated diseases and disorders by modulating the expression or secretion of IL-4, IL-5 and IL-13 using interferon lambda (IFN-λ). For Th2-associated diseases and disorders, cells of a patient having a Th2-associated disease or disorder are treated ex vivo, with IFN-λ and returned to the patient. The present invention also provides a method of ex vivo treatment, in conjunction with co-administration of IFN-λ | 02-20-2014 |
20140057960 | NOVEL REPRESSOR ON IFN-LAMBDA PROMOTER AND SIRNA AGAINST ZEB1 AND BLIMP-1 TO INCREASE IFN-LAMBDA GENE ACTIVITY - The present invention is directed to the identification of a novel repressor located between ˜1.2 kb to ˜1.6 kb from the translation start site of the IFN-λ1 promoter. The present invention provides a method of using siRNAs against ZEB1 (binds to the repressor region) and BLIMP-1 (binds outside the repressor region) and increases the promoter activity of IFN-λ1 (i.e., increases the production of IFN-λ1 protein). siRNAs against ZEB1 mRNA or BLIMP-1 mRNA increase IFN-λ1 gene activity. There is provided a therapeutic application of siRNAs against ZEB1 and BLIMP-1 mRNAs in treating a mammal (including a human) by increasing the production of IFN-λ1 protein that promotes an anti-viral response as well as treats asthma diseases and colon diseases. | 02-27-2014 |
20140187602 | Anti-Sense Oligonucleotides Targeted Against Exon 9 of IL-23R alpha Gene and Method of Using Same to Induce Exon Skipping and to Treat Inflammatory Bowel Diseases - The present invention relates to anti-sense oligonucleotides (AONs) used to induce exon 9 skipping in IL-23Rαgene. Exon 9 skipping of the IL23Rα gene ultimately causes specific induction of a novel soluble truncated IL-23Rα (Δ9) protein, characterized by a lack in a transmembrane domain and has a unique eight (8) amino acids (GLKEGSYC) at its C-terminus end as a result of frame-shift. The present invention provides a utility application of the use of AONs to induce production of a Δ9 protein which inhibits IL-23R-mediated cell signaling. More particularly, Δ9 protein blocks STAT3 formation as well as Th17 maturation. There is provided a therapeutic application of AONs in treating a mammal such as a human patient inflicted with Crohn's disease. | 07-03-2014 |
20140272994 | METHODS AND REAGENTS THAT SPECIFICALLY DETECT, DISTINGUISH AND QUANTIFY IFN-LAMBDA2 mRNA FROM IFN-LAMBDA3 mRNA IN HUMANS - The present invention provides a method of specifically detecting IFN-λ2 mRNA or IFN-λ3 mRNA. There is provided a qRT-PCR method specifically detecting, discriminating and quantifying IFN-λ2 and IFN-λ3 mRNA in a biological sample obtained from a human. There is provided qRT-PCR methods and primers and probes that specifically detect IFN-λ2 mRNA but not IFN-λ3 mRNA and vice versa in humans in order to detect, quantify and discriminate IFN-λ2 mRNA and IFN-λ3 mRNA. | 09-18-2014 |
20140350072 | NOVEL REPRESSOR ON IFN-LAMBDA PROMOTER AND SIRNA AGAINST ZEB1 AND BLIMP-1 TO INCREASE IFN-LAMBDA GENE ACTIVITY - The present invention is directed to the identification of a novel repressor located between ˜1.2 kb to ˜1.6 kb from the translation start site of the IFN-λ1 promoter. The present invention provides a method of using siRNAs against ZEB1 (binds to the repressor region) and BLIMP-1 (binds outside the repressor region) and increases the promoter activity of IFN-λ1 (i.e., increases the production of IFN-λ1 protein). siRNAs against ZEB1 mRNA or BLIMP-1 mRNA increase IFN-λ1 gene activity. There is provided a therapeutic application of siRNAs against ZEB1 and BLIMP-1 mRNAs in treating a mammal (including a human) by increasing the production of IFN-λ1 protein that promotes an anti-viral response as well as treats asthma diseases. | 11-27-2014 |