24 results about "Graft rejection" patented technology

This invention provides an antibody composition with improved stability, exhibiting reduced fragmentation of the antibody polypeptide chain during manufacturing and subsequent storage. [Solution] This disclosure relates to improved compositions and methods for treating T cell-mediated diseases and disorders (e.g., autoimmune disorders, graft-versus-host diseases, and graft rejection). Provided are antibody-containing anti-αβTCR binding polypeptides comprising at least one amino acid substitution or modification that enhances the stability of the binding polypeptide by reducing fragmentation of the light chain variable region. Methods provided herein generally involve administering an effective amount of a stabilized, humanized binding polypeptide specific to the alpha-beta T cell receptor (αβTCR) to a subject in need thereof.

The present invention provides novel drug-linker conjugates and antibody-drug conjugates of imidazo quinoline amine derivatives, which have agonistic activity against Toll-like receptors (TLRs), in particular TLR7 and / or TLR8, also provided are pharmaceutical compositions and methods of treatment against certain diseases or conditions mediated by or associated with TLR7 and / or TLR8 (e.g., graft rejection, autoimmunity, inflammation, allergy, asthma, infection, sepsis, cancer, and immunodeficiency).

Provided is a modified regulatory T cell capable of recognizing cells of the liver, capable of treating and / or preventing transplant rejection or immune-mediated damage, and capable of promoting regeneration of cells of the liver.SOLUTION: The present invention provides engineered regulatory T cells (Tregs) comprising a chimeric antigen receptor (CAR), wherein said CAR comprises an antigen recognition domain that specifically binds to the asialoglycoprotein receptor (ASGR). The invention also provides a method of promoting liver tissue repair and / or regeneration in a subject, said method comprising administering to said subject a modified Treg comprising a CAR, or a pharmaceutical composition comprising said modified Treg, wherein said CAR comprises a liver-specific antigen recognition domain.SELECTED DRAWING: None

The present invention relates to the role of purinergic receptors and ATP in T cell activation and autocrine system signaling. In one embodiment, the present invention provides a method of preventing or treating diabetes by administering a therapeutically effective inhibitor of ATP to a subject. In another embodiment, the present invention provides a method of preventing or treating fibrosis by administering a P2X7R soluble fusion protein. In another embodiment, the present invention provides a method of preventing or treating graft rejection by administering an inhibitor of P2X receptor signaling.

Clinical detection or diagnosis of transplant rejection currently utilizes various methods that rely on qualitative rather than quantitative data, or quantitative data that has low sensitivity and / or has a high rate of operator error. Provided herein are methods for identifying kidney transplant rejection in patents that is automated and consistent for the user. Further described herein are cut-offs for transplant biomarkers that relate to renal transplantation stability or rejection.

The invention relates to an anti-immunological rejection FK506 (at) ZIF-8 / HTCC ophthalmic gel and a preparation method thereof, FK506 and a zeolite imidazole skeleton (ZIF-8) are combined to prepare FK506 loaded nanoparticles (FK506 (at) ZIF-8), and quaternized chitosan is innovatively used as a sol of the FK506 (at) ZIF-8 to prepare the ophthalmic gel for use. The problems that a novel potent immune preparation tacrolimus administration mode is short in drug retention time, fast in metabolism, poor in cornea permeability and insoluble in water, and consequently the bioavailability of the FK506 eye drops is low are solved. Compared with an FK506 direct administration mode, the administration mode of the novel nanoparticle drug-loaded ophthalmic gel is higher in drug utilization rate, has a treatment effect on corneal transplantation immunological rejection, and delays the occurrence and development of transplantation rejection.

The invention discloses a chimeric receptor with an anti-transplant rejection function and an engineering cell for expressing the chimeric receptor, and further relates to a method for resisting tumors and transplant immunological rejection, in particular to a method for resisting NK cell immunological rejection. The invention also relates to cell therapy.

Provided herein are methods and compositions for treating kidney-related disease conditions and complications, such as Berger's disease, and for preventing transplant rejection. For example, the present disclosure describes a method of improving function of a transplanted kidney in a subject in need thereof, wherein the method comprises administering to the subject a therapeutically effective amount of an antibody or antigen-binding fragment thereof that specifically binds CD40 ligand.

The present disclosure relates to materials and methods for evaluation of transplant rejection in a subject. In particular. provided herein are synthetic scaffolds and methods of use thereof for early diagnosis of transplant rejection in a subject.

An antibody or antigen-binding fragment thereof that specifically binds to TNFR2 with high affinity is provided. The invention also provides a nucleic acid molecule for coding the antibody or the antigen binding fragment thereof, an expression vector and a host cell for expressing the antibody or the antigen binding fragment thereof, and a production method of the antibody or the antigen binding fragment thereof. The provided antibodies can mediate proliferation and activation of Treg cells, and can be used to treat autoimmune diseases, asthma, anaphylaxis, graft versus host disease, graft rejection, and a variety of other immune diseases.

This disclosure provides small molecule pyrrole-3-carboxamide compounds, compositions thereof, and methods of using them to modulate DCAF1 and treat a variety of diseases, disorders or conditions associated with DCAF1, such as neurological disorders like Alzheimer's disease, Parkinson's disease or Huntington's disease, transplant rejection, AIDS-related Kaposi's sarcoma, and particularly cancer.

New methods for assessing the status of transplant rejection in transplant recipients, such as kidney transplant recipients, are disclosed. The diagnostic methods utilize the measurement of TCR subunit repertoire diversity to identify stable subjects, subjects undergoing cell-mediated rejection processes, and subjects undergoing antibody-mediated rejection processes. The proportion of unique TCR alpha and beta subunit sequences to the total unique TCR subunit sequences (total sequences of alpha, beta, delta, and gamma subunits) provides a diagnostic measure that can identify stable subjects, subjects undergoing cell-mediated rejection processes, and subjects undergoing antibody-mediated rejection processes. If antibody-mediated rejection or cell-mediated rejection is detected, treatment methods include administration of appropriate therapy.

In the various aspects and embodiments, the present disclosure provides cell populations or cell “banks” thereof (e.g., cell collections) to provide immune compatible, allogeneic cell therapies covering global, ethnic, and disease-specific populations. In the various aspects and embodiments, the cell banks and progeny thereof maintain sufficient HLA Class I and HLA Class II functionalities, while facilitating patient matching to prevent or reduce graft versus host disease (GVHD) or graft rejection. The disclosure further provides methods for creating the cell banks by gene editing, and methods for cell therapy involving cells or tissues derived from the cell banks (including but not limited to hematopoietic stem cells, or “HSCs”, progenitors, or progenies thereof).

The present application provides a kind of CD47 mutant and its application, wherein CD47 mutant includes the amino acid sequence of partial amino acid sequence of CD47 and glycosyl phosphatidyl inositol (GPI) connection signal.The CD47 mutant is obtained by removing potential cell survival inhibition, blood flow and angiogenesis inhibition and other negative effect signal transduction sequences (transmembrane region and intracellular region) in CD47, while the beneficial functional segment (extracellular IgV domain) involved in inhibiting the phagocytosis of myeloid cells and its cytotoxic activity in CD47 sequence is fused with GPI membrane anchor connection signal sequence from human decay accelerating factor (DAF) protein.The obtained CD47 mutant can protect cells and organ transplants from being mediated by myeloid cells and other SIRP alpha positive immune cells with equal efficacy to wild type CD47, and at the same time eliminates the negative effects of wild type CD47.

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.

Provided herein are compositions comprising microgels conjugated to a protease-resistant C-X-C motif chemokine 12 (CXCL12) polypeptide, a Fas ligand (FasL) polypeptide, or both. Methods of making the microgel compositions as well as pharmaceutical compositions comprising thereof are also contemplated herein. Provided herein are also methods of inducing an immune privileged environment for transplantation, methods of treating or preventing graft rejection in a subject in need thereof, as well as methods of treating Type 1 diabetes.

The present invention relates to double stranded oligonucleotides that are complementary to JAK1, leading to modulation of the expression of JAK1. Modulation of JAK1 expression is beneficial for a range of medical disorders including dry eye disease, inflammatory bowel disease, organ transplant rejection, graft-versus-host disease, multiple sclerosis, rheumatoid arthritis (RA), juvenile idiopathic arthritis, psoriasis, dermatitis, diabetic nephropathy, systemic lupus erythematosus (SLE), cancer, myelofibrosis, and asthma. Also included are compositions comprising the double stranded oligonucleotide and methods of treatment using the double stranded oligonucleotide.

The present invention relates to double stranded oligonucleotides that are complementary to JAK1, which elicit modulation of the expression of JAK1. Modulation of JAK1 expression is advantageous for a range of medical conditions including inflammatory bowel disease, organ transplant rejection, graft versus host disease, multiple sclerosis, rheumatoid arthritis (RA), juvenile idiopathic arthritis, psoriasis, dermatitis, diabetic nephropathy, systemic lupus erythematosus (SLE), dry eye disease, cancer, myelofibrosis, and asthma. The invention also includes compositions comprising the double-stranded oligonucleotides and methods of treatment using the double-stranded oligonucleotides.

The present invention relates to an isolated muropeptide of formula (I) GlcNAc-MurNAc-X1-Glu-mDAP-(Ala)Y1-(X2)Y2 as well as peptidoglycans (PG) comprising it and to a composition comprising at least one muropeptide and / or at least one PG and to the implementation of the muropeptide, peptidoglycan or composition in the prevention and / or treatment, in an individual in need thereof, of an immune disorder selected from the group consisting of an inflammatory disorder, graft-versus-host disease (GVHD) and graft rejection; or of an infection; or of a metabolic disorder or of a cancer.

The invention discloses a fusion protein with an anti-transplant rejection function and an engineering cell for expressing the fusion protein, and further relates to a method for resisting transplant immunological rejection, in particular to a method for resisting NK (Natural Killer) cell immunological rejection.

To provide a pharmaceutical composition for use in a method for predicting the responsiveness of a subject having an autoimmune disease or condition, transplant rejection, or graft versus host disease to an immunotherapeutic agent.SOLUTION: The pharmaceutical composition comprises a labeled CD8-binding agent comprising a heavy chain variable domain (VHH domain) of a heavy chain antibody, wherein the method comprises a) administering the labeled CD8-binding agent to the subject; and b) detecting binding of the labeled CD8-binding agent to CD8 + T cells in a diseased tissue of the subject, wherein detection of the binding indicates that the subject is likely to respond to the immunotherapeutic agent.SELECTED DRAWING: None

The present disclosure is related to improved compositions and methods for treating T-cell-mediated diseases and disorders (e.g., autoimmune disorders, graft-versus-host-disease, and graft rejection). Provided are anti-αβTCR binding polypeptides, including antibodies, which comprise at least one amino acid substitution or modification that increases the stability of the binding polypeptide by reducing fragmentation of the light chain variable region. The methods provided herein generally involve administering to a subject in need thereof an effective amount of a stabilized, humanized binding polypeptide that is specific to the alpha beta T-cell receptor (αβTCR).

The invention relates to the technical field of biochemistry, and particularly discloses a heparin binding protein-based transplant rejection risk early warning method, which comprises the following steps of: obtaining a biological sample of a transplant recipient; detecting the concentration of HBP in the biological sample; comparing the HBP concentration with a preset reference value; if the HBP concentration is higher than the reference value, prompting that a transplant rejection risk exists; by dynamically monitoring the concentration of the heparin-binding protein, the kit can prompt the occurrence of infection after organ transplantation earlier compared with a traditional inflammatory marker, has high sensitivity and specificity, and is beneficial to realizing evaluation and timely intervention of the immune state of a patient before typical clinical symptoms or microbiological evidences do not appear in the early stage of infection.

Disclosed herein are computer-implemented systems, kits, and methods for determining the amount of nucleic acid derived from a contributor in a biological sample from a transplant recipient, the amount of nucleic acid derived from two or more genetically distinct contributors. The determined amount of nucleic acid derived from a contributor can be useful for monitoring the status of the transplant, for example, to assess the risk of transplant rejection. In some examples, the two or more genetically distinct contributors can include the transplant recipient, the fetus, and the transplant donor. In some examples, the two or more genetically distinct contributors can include the transplant recipient, the first transplant donor, and the second transplant donor. For example, the systems and methods determine an estimated percentage of nucleic acid derived from a contributor and / or an estimated percentage of nucleic acid derived from the fetus.