25 results about "CD59" patented technology

To provide methods and kits for inhibiting inflammasome activation in cells of a subject or an inflammation-affected eye in the subject.SOLUTION: A composition, which comprises a nucleotide sequence encoding a membrane independent CD59 protein operably linked to a promoter for expression and secretion of the membrane independent CD59 protein in cells of a subject or an inflammation-affected eye in the subject or a soluble CD59 protein and inhibits inflammasome activation, is administered to the subject.SELECTED DRAWING: None

The invention belongs to the technical field of biological medicines, and particularly relates to application of chenodeoxycholic acid in preparation of drugs for treating allergic diseases. It is found that CDCA can effectively inhibit pyroptosis and secretion of proinflammatory factors, expression of complement inhibition proteins CD46, CD55 and CD59 is remarkably up-regulated, expression of the complement inhibition proteins CD46, CD55 and CD59 is finally promoted, and occurrence and development of allergic diseases are effectively relieved. In a mouse model, CDCA can significantly improve OVA-induced food allergy symptoms, and has application prospects in treatment of allergic diseases.

The invention relates to the field of oncology, in particular to application of a cancer immunotherapy target and a diagnosis and prognosis prediction biomarker. Wherein at least one marker in the EGFR / Wnt / beta-catenin-LINC00973-miRNA-CD55 / CD59 pathway can be used for evaluating the sensitivity or the prognosis of the cancer immunotherapy.

The described invention provides method for treating a complement disorder such as age-related macular degeneration (AMD) in a subject, comprising administering a pharmaceutical composition into an affected eye of a subject by ocular injection, wherein the composition comprises a nucleic acid encoding a soluble CD59 (sCD59) protein operably linked to a promoter, wherein the nucleic acid encoding sCD59 is packaged into a delivery vector and wherein the administering results in expression and secretion of the sCD59 protein by cells of the affected eye and the expression results in treatment of affected cells in the affected eye.

The present invention relates to an oncolytic virus co-expressing the complement regulatory proteins CD55 and CD59. The oncolytic virus of the present invention maintains efficacy even upon intravenous injection, and thus, it may be applied to the therapy for various solid carcinomas and metastatic cancers as well as superficial solid cancers. In addition, the oncolytic virus of the present invention acquires resistance to the attack of human complement system by expressing a complement regulatory protein on the surface of the virus, and thus, it is stable in blood, and it maintains stable oncolytic activity upon intravenous injection, and thus, it may reduce the dose of the virus to minimize adverse effects of anticancer agents. Therefore, the oncolytic virus of the present invention may be advantageously used for prevention or treatment of cancer.

The present invention relates to anti-cancer viruses that co-express complement regulatory proteins CD55 and CD59. Since the anti-cancer virus of the present invention can maintain its curative effect even when intravenously injected, the anti-cancer virus can also be applied to the treatment of various solid cancers and metastatic cancers in addition to superficial solid cancers. Furthermore, the anti-cancer virus of the present invention obtains resistance to attacks of an in-vivo complement system by expressing complement regulatory protein on the surface of the virus, thereby being stable in blood and maintaining stable anti-cancer activity during intravenous injection, thereby reducing the application amount of the virus to reduce the side effects of anti-cancer drugs as much as possible. Therefore, the anti-cancer virus of the present invention can be used for preventing or treating cancer.

Applicants engineered peptide-modified AAV9 capsids for system-wide enhanced organ transduction by directly engineering a binding interaction with the human GPI-linked glycoprotein CD59. Adeno-associated vimses (AAVs) are used by numerous approved and investigational gene therapies. However, native AAVs have limited tissue tropisms and have comparatively low extrahepatic delivery efficiencies. While capsid engineering has largely focused on targeting specific organs, treating multisystem disorders requires efficient gene delivery to many organs. Here Applicants describe novel engineered capsids that bind CD59.

The invention belongs to the technical field of biological medicine, and particularly relates to a recombinant adeno-associated virus vector for delivering anti-VEGF (vascular endothelial growth factor) and complement protein co-expression and application of the recombinant adeno-associated virus vector. The co-expression system is constructed by adopting a genetic engineering technology, and efficient co-expression and accurate shearing of two treatment proteins are realized by inserting an F2A polypeptide connecting sequence between an Aflibercept protein coding sequence and a CD59 protein coding sequence.

A method of promoting T cell proliferation and function by intracellular CD59 is provided, comprising silencing the CD59 gene in a T cell. The invention also provides a nucleic acid molecule interfered by the CD59 gene, and a target sequence in the CD59 gene is shown as SEQ ID NO: 1. Gene editing is carried out through shRNA (short hairpin ribonucleic acid), siRNA (small interfering ribonucleic acid) or a CRISPR-Cas9 (clustered regularly interspaced short palindromic repeats-associated protein 9) technology, and human CD59 gene expression is silenced by sgRNA of a specific targeting CD59 gene. The constructed lentiviral vector realizes hereditary silencing of the CD59 gene in the T cell, and the expression level of the CD59 in the edited T cell is obviously reduced, so that the cell proliferation is obviously accelerated, the cell factor release is obviously increased, the function is obviously enhanced, and a new strategy is provided for the treatment of tumors and immune diseases.

The invention discloses a platelet subgroup as well as a preparation method and application thereof. A surface labeled molecule CD59 or CD59a of the platelet subgroup is positive. The platelet subgroups enriched by the identified surface marker molecules can remarkably improve the skin tissue repair efficiency, so that a more effective repair promoting strategy is provided for patients to relieve health pressure and economic burden caused by wounds.

The present invention relates to an oncolytic virus co-expressing the complement regulatory proteins CD55 and CD59. The oncolytic virus of the present invention maintains efficacy even upon intravenous injection, and thus, it may be applied to the therapy for various solid carcinomas and metastatic cancers as well as superficial solid cancers. In addition, the oncolytic virus of the present invention acquires resistance to the attack of human complement system by expressing a complement regulatory protein on the surface of the virus, and thus, it is stable in blood, and it maintains stable oncolytic activity upon intravenous injection, and thus, it may reduce the dose of the virus to minimize adverse effects of anticancer agents. Therefore, the oncolytic virus of the present invention may be advantageously used for prevention or treatment of cancer.

The present invention relates to an anticancer virus that co-expresses the complement regulatory proteins CD55 and CD59. The anticancer virus of the present invention maintains its efficacy even after intravenous injection, making it suitable for the treatment of various solid carcinomas and metastatic cancers in addition to superficial solid cancers. Furthermore, by expressing complement regulatory proteins on the viral surface, the anticancer virus of the present invention acquires resistance to attack by the endogenous complement system, is stable in the blood, and maintains stable anticancer activity upon intravenous injection, thereby reducing the viral dosage and minimizing the side effects of anticancer drugs. Therefore, the anticancer virus of the present invention can be useful for the prevention or treatment of cancer.

This document provides methods and materials involved in reducing cardiac xenograft rejection. For example, methods and materials for preparing transgenic pigs expressing reduced or no endogenous Sda or SDa-like glycans derived from the porcine β1,4 N-acetyl-galactosaminyl transferase 2 (B4GALNT2) glycosyltransferase and / or reduced or no endogenous α-Gal antigens, methods and materials for modifying the xenograft recipient's immunological response to non-Gal antigens (e.g. CD46, CD59, CD9, PROCR, and ANXA2) to reduce cardiac xenograft rejection, and methods and materials for monitoring the progress of xenotransplant immunologic rejection are provided.

The invention pertains to treating a cognitive impairment, for example, an aging-associated cognitive impairment. In certain aspects, a sample obtained from a subject is assayed for the ratio between the levels of any two proteins selected from: DLL1, SMOC1, CD59, TSTD1, STAT3, POLD4, PARP11, LEFTY2, UNC5B, C5, C5.C6, ASH2L, INHBB, RSP3, VAV3, SIRT3 and SERPINB8. A subject may be having or suspected of having a cognitive impairment. The cognitive impairment can be caused by a neurodegenerative disease, such as Alzheimer's disease. A subject may be identified as likely or not likely to respond positively to the plasma exchange therapy based on the ratio between the levels of measured proteins. In certain aspects, methods for treating a cognitive impairment in the subject comprise administering a plasma exchange therapy comprising a full and / or low volume plasma exchange. Also provided are kits suitable for performing such methods.

Disclosed herein are polynucleotides encoding fusion proteins, the fusion protein comprising a vaccinia virus envelope protein, such as A13 or a portion thereof, and at least one complement control protein, or a functional fragment thereof, such as CD35, CD55, CD59, CD46, CR1, Factor H, VCP, MOPICE, SPICE, and CCPH. Modified vaccinia virus vectors and vaccinia virus virions are also disclosed, as are therapeutic uses and methods for the treatment of cancer and / or proliferative diseases or disorders.

This invention relates to an antibody composition for detecting PNH clones and its application. The antibody composition comprises a first antibody group, a second antibody group, and a third antibody group. The first antibody group includes a CD235a antibody, the second antibody group includes a CD235a antibody and a CD59 antibody, and the third antibody group includes a FLAER antibody, a CD157 antibody, a CD15 antibody, a CD64 antibody, and a CD45 antibody. In this invention, the three antibody groups can be used to identify mature erythrocytes, neutrophils, and monocytes in peripheral blood. PNH clones in erythrocytes are detected using CD235a and CD59, and PNH clones in neutrophils and monocytes are detected using FLAER and CD157 antibodies. The FLAER antibody directly binds to the GPI anchor structure, and the CD157 antibody, as an additional GPI anchor protein indicator, can detect potentially missed microclones.

This disclosure relates to methods for detecting a level of expression of one or more genes (or proteins) in a subject having or suspected of having cancer, and optionally treating the subject with an adenosine pathway antagonist, for example an adenosine A2A receptor (ADORA2A) antagonist, to treat the cancer. The genes (or proteins) include, without limitation, CD68, CD163, LBP, CCL2, CCL3, CCL7, CCL24, CCNE1, CD 14, CD300E, CD86, CD93, CLEC5A, CSF3, CXCL1, CXCL2, CXCL3, CXCL5, CXCL6, CXCL8, DFNA5, ECEL1, EPB41L3, EHF, FUT7, GALM, GBP6, GPR157, HAS1, IL1A, IE-1β, IL23, IL24, IL5, IL6, IL8, INHBA, LAP3, LAYN, LOC100505585, MRPL11, NID1, OST4, PADI2, PID1, PLAUR, PPBP, PTGS2, RHCG, SERPINB2, SLC11A1, SLC7A7, SPON1, ST6GALNAC2, TBX21, THBS1, C1R, C1S, C4BPA, CCL11, CCL20, CXCL16, CXCL2, HAMP, HSD11B1, IT GAM, LIF, SAA1, TFRC, TLR5, TNFSF14, TREM2, APP, ATG10, BCL2, CCL15, CD24, CD46, CD59, CREB5, CX3CL1, CXCL14, CYFIP2, DEFB1, DPP4, ECSIT, EPCAM, IFIT1, IGF1R, ITGA6, ITGB3, MAP2K4, MAPK1, MASP1, PPARG, RORC, SPA17, STAT5B, TOLLIP, AKT3, BMI1, CD 164, CD34, CDH5, CREB1, DOCK9, ENG, HMGB1, ITGA1, JAM3, MAF, MAPK3, MAPK8, MCAM, MFGE8, NOTCH1, NRP1, PRKCE, SMAD2, TAL1, THY1, TNFSF12, TRAF6, TXNIP, VEGFA, S100A8, and / or WDR830S.

The invention pertains to treating a cognitive impairment, for example, an aging-associated cognitive impairment. In certain aspects, a sample obtained from a subject is assayed for the ratio between the levels of any two proteins selected from: DLL1, SMOC1, CD59, TSTD1, STAT3, POLD4, PARP11, LEFTY2, UNC5B, C5, C5.C6, ASH2L, INHBB, RSP3, VAV3, SIRT3 and SERPINB8. A subject may be having or suspected of having a cognitive impairment. The cognitive impairment can be caused by a neurodegenerative disease, such as Alzheimer's disease. A subject may be identified as likely or not likely to respond positively to the plasma exchange therapy based on the ratio between the levels of measured proteins. In certain aspects, methods for treating a cognitive impairment in the subject comprise administering a plasma exchange therapy comprising a full and / or low volume plasma exchange. Also provided are kits suitable for performing such methods.

The application discloses application of a cancer immunotherapy target and a diagnosis, prognosis prediction biomarker, and determines detection of cancer cells of a patient or blood of the patient to contain: an EGFR activation level, a Wnt pathway activation level, an activated beta-catenin level, a long non-coding RNA LINC00973 expression level, a LNC1574203 expression level, a CD55 protein and mRNA expression level, a CD59 protein and mRNA expression level, and a CD73 protein and mRNA expression level, which are higher than reference levels, are used for diagnosis, prognosis prediction and treatment of cancer.

Applicants engineered peptide-modified AAV9 capsids for system-wide enhanced organ transduction by directly engineering a binding interaction with the human GPI-linked glycoprotein CD59. Adeno-associated vimses (AAVs) are used by numerous approved and investigational gene therapies. However, native AAVs have limited tissue tropisms and have comparatively low extrahepatic delivery efficiencies. While capsid engineering has largely focused on targeting specific organs, treating multisystem disorders requires efficient gene delivery to many organs. Here Applicants describe novel engineered capsids that bind CD59.

The present invention relates to a transgenic cloned pig for xenotransfusion and xenotransplantation in which the porcine GGTA1, CMAH, iGb3s, and β4GalNT2 genes are deleted and the human CD59 gene is knocked in, and a method for producing same. By inducing expression of the human CD59 gene in a transgenic pig, which improves the existing antigen-antibody mediated immune rejection response, the complement mediated immune rejection response was reduced, and expression of the human CD59 gene was confirmed in red blood cells, and therefore, the pig may be effectively used for xenotransfusion and xenotransplantation.

Applicants engineered peptide-modified AAV9 capsids for system-wide enhanced organ transduction by directly engineering a binding interaction with the human GPI-linked glycoprotein CD59. Adeno-associated vimses (AAVs) are used by numerous approved and investigational gene therapies. However, native AAVs have limited tissue tropisms and have comparatively low extrahepatic delivery efficiencies. While capsid engineering has largely focused on targeting specific organs, treating multisystem disorders requires efficient gene delivery to many organs. Here Applicants describe novel engineered capsids that bind CD59.

Disclosed herein are polynucleotides encoding fusion proteins, the fusion proteins comprising a vaccinia virus envelope protein, such as A13 or part thereof and at least one complement regulatory protein, such as CD35, CD55, CD59, CD46, CR1, Factor H, VCP, MOPICE, SPICE and CCPH, or a functional fragment thereof. Modified vaccinia virus vectors and vaccinia virus virions are also disclosed, as are therapeutic uses and methods for treatment of cancers and / or proliferative diseases or disorders.

The present invention relates to an oncolytic virus co-expressing the complement regulatory proteins CD55 and CD59. The oncolytic virus of the present invention maintains efficacy even upon intravenous injection, and thus, it may be applied to the therapy for various solid carcinomas and metastatic cancers as well as superficial solid cancers. In addition, the oncolytic virus of the present invention acquires resistance to the attack of human complement system by expressing a complement regulatory protein on the surface of the virus, and thus, it is stable in blood, and it maintains stable oncolytic activity upon intravenous injection, and thus, it may reduce the dose of the virus to minimize adverse effects of anticancer agents. Therefore, the oncolytic virus of the present invention may be advantageously used for prevention or treatment of cancer.

Compositions and kits for diagnosing and prognosing Alzheimer's Disease (AD) in a human patient include a binding agent such as a monoclonal antibody for a biomarker conjugated to a detectable moiety such as a fluorophore, wherein the biomarker is chosen from CD163, CD91, CD59, MerTK and other phagocytosis-related molecules. Further compositions and kits employ panels of fluorophore-conjugated monoclonal antibodies for biomarkers including scavenger receptors. Methods for determining the relative expression of biomarkers, diagnosing AD, and determining the efficacy of AD therapeutic candidates such as phagocytosis-promoting agents and scavenger receptor agonists also appear.