10 results about "Interferon receptor" patented technology

The invention discloses a pig IFNAR2 protein mutant, which is characterized in that the 399th site in the amino acid sequence of the pig IFNAR2 protein is mutated from glycine to alanine, and the amino acid sequence of the pig IFNAR2 protein is as shown in SEQ ID NO. 1. The invention provides a specific cleavage site of ASFV protease pS273R, and the site is mutated through a gene editing technology so as to block the cleavage of pig IFNAR2 by the pS273R and improve the ability of pigs to resist African swine fever virus infection. By blocking ASFV from damaging type I IFN mediated JAK-STAT signal activation, on the basis of retaining pig autoimmune performance, higher specificity and higher efficiency are achieved, negative effects of genetic engineering on pig growth performance and reproductive performance can be greatly reduced, and biosafety is higher.

This invention provides an application of type I interferon signaling pathway inhibitors in the preparation of drugs for treating age-related cataracts. By inhibiting type I interferon receptors, it can precisely intervene in the aging mechanism of lens epithelial cells, block the transmission of aging signals, and directly improve lens transparency, exhibiting higher therapeutic efficacy and targeting. The use of IFNAR inhibitors can effectively reverse the aging phenotype caused by STEAP3 deficiency, restore the proliferative capacity of lens epithelial cells, thereby maintaining lens transparency, significantly reducing surgical risks, and providing patients with an early intervention opportunity, delaying the onset and progression of cataracts. IFNAR inhibitors, through precise intervention in specific signaling pathways, have more significant therapeutic effects, and due to their targeting, have fewer side effects and are safer. They can not only improve existing cataracts but also play a preventive and delaying role in the early stages of cataracts. For patients with mild cataracts, the use of type I interferon receptor inhibitors can avoid premature surgical treatment, reducing patient dependence on surgery and also reducing the costs and risks associated with surgery.

The present disclosure provides interferon (IFN) receptor antagonists. The IFN receptor antagonists disclosed herein comprise an anchoring moiety, an IFN masking moiety, an IFN moiety, and a separating moiety, such as a targeting moiety that recognizes an antigen associated with a cell expressing a type 1 interferon receptor and anchors the IFN receptor antagonist to such cell. The disclosure further provides pharmaceutical compositions comprising the IFN receptor antagonists, and methods of using the IFN receptor antagonists in inhibition of IFN signaling, including methods of treatment. Also disclosed are nucleic acids encoding the IFN receptor antagonists, recombinant cells expressing the IFN receptor antagonists, and methods of producing the IFN receptor antagonists.

Provided is a human a interferon receptor binding-related site mutant IFN-α2-EIFK. The mutant has stronger anti-hepatitis B virus activity than IFN-α2, and has no cytotoxic effect at an antiviral concentration. An anti-hepatitis B virus drug can be prepared therefrom.

The invention relates to the field of biological medicine, and relates to application of an interferon receptor 1 monoclonal antibody in preparation of a medicine for treating neuromyelitis optica pedigree diseases and a medicine composition. The antibody regulates immune response by inhibiting abnormal activation of an I-type interferon signal channel and down-regulating interferon stimulation gene expression, so that central nervous system inflammation and demyelination injury are relieved. The humanized IFNAR1 monoclonal antibody is independently used; the compound is combined with a B cell targeting drug to synergistically inhibit B cell activation and antibody secretion; and a bispecific antibody targeting IFNAR1 and a transferrin receptor is constructed, so that the ability of the drug to pass through the blood brain barrier is enhanced, and the concentration of the drug in the brain is improved. In-vivo and in-vitro experiments prove that the treatment scheme can effectively reduce the size of the focus of the NMOSD model and improve the neurological function, and a new precise treatment strategy is provided for AQP4 antibody positive patients.

The invention belongs to the technical field of microbial genetic engineering, and discloses a method for detecting binding capacity of poultry interferon and interferon receptor in plants and application thereof, the method comprises the following steps: S1, respectively constructing optimized interferon gene and interferon receptor gene to the N terminal and C terminal of a plant expression vector to obtain a plant expression vector; obtaining a recombinant expression vector; s2, respectively transforming the recombinant expression vectors into agrobacterium host bacteria to obtain genetically engineered bacteria; s3, injecting the genetically engineered bacterium into tobacco, and culturing the tobacco injected with the bacterium liquid, so that the interferon and the interferon receptor are expressed in the tobacco; and S4, capturing a fluorescence signal by using a CCD imaging system, analyzing the fluorescence intensity of a specific region by using image analysis software, and detecting the interaction strength relationship between the interferon protein to be detected and the interferon receptor protein through the fluorescence intensity. The method is convenient to operate, the detection result is visual, the workload can be greatly reduced, and the detection efficiency is improved.

This disclosure provides immune cells (e.g., CAR-T cells) comprising a chimeric antigen receptor and / or an engineered immune cell receptor, that are deficient in interferon y receptor (IFNyR) expression and / or signaling, and methods of use thereof, wherein the CAR-immune cell have increased persistence.

This invention provides a method and unit dose for the treatment of type I IFN-mediated diseases. [Solution] The present invention provides a unit dose for subcutaneous administration of a type I IFN receptor (IFNAR1) inhibitor in a dose greater than 105 mg (>) and less than 150 mg (<), specifically a human monoclonal antibody specific to IFNAR1, or optionally a modified IgG1 class human monoclonal antibody, and a method comprising subcutaneously administering the unit dose to a subject having a type I interferon (IFN)-mediated disease.

An interferon α2b mutant, and a fusion polypeptide and polypeptide construct comprising same. The fusion polypeptide or polypeptide construct comprising the interferon α2b mutant has weakened affinity to an interferon receptor, reduced off-target toxicity, and a tumor killing effect.

This disclosure relates to methods and compositions for the treatment of SLE. Specifically, this disclosure relates to methods including the administration of type I IFN receptor inhibitors.