17 results about "Immune Evasions" patented technology

The present invention provides compositions for the prevention and treatment of genital herpes, comprising nucleoside modified mRNAs that encode herpes simplex virus (HSV) glycoproteins, including those involved in virus entry and immune evasion, and methods of use thereof.

Therapeutic agents that can place bulky proteins, such as CD45, CD148, and CD43, at the center of the cellular interface between graft cells and CD45-positive host effector cells (e.g., T cells, NK cells, B cells, or dendritic cells) are disclosed, as are methods of their use and products made with such therapeutic agents. The therapeutic agents prevent or inhibit the formation of functional immunological synapses (including physiological SMACs). They also result in the continuous dephosphorylation of signaling pathways.

This invention provides an H3N2 influenza mRNA vaccine targeting the tandem HA and NA proteins and its preparation method, relating to the field of vaccine preparation technology. The H3N2 influenza mRNA vaccine is obtained by linking the conserved amino acid sequences of HA and NA of H3N2 with GGGSGGGSGGGSGGGS, and the amino acid sequence of the H3N2 influenza mRNA vaccine is shown in SEQ ID NO.1, and the nucleic acid sequence is shown in SEQ ID NO.2. This invention overcomes the shortcomings of existing technologies, improves the protective effect of the vaccine against H3N2 influenza, and enables it to better cope with immune evasion from the latest emerging H3N2 variants.

The invention belongs to the technical field of gene engineering, and particularly relates to a construction method and application of a recombinant vector based on bCoro1a gene 3 'UTR editing. The recombinant vector consists of an upstream homologous arm of a targeting site, 3 'UTR inserted into a target sequence, 200bp of a nucleotide tailing signal of bCoro1a, a selection marker and a downstream homologous arm of the targeting site; the targeting site is the 29 or 70 site of the 3 'UTR of the bCoro1a gene; the sequence of the 3 'UTR of the bCoro1a gene is as shown in SEQ ID NO. 48; the selection marker comprises enhanced green fluorescent protein and puromycin, the bCoro1a 3 'UTR edited gene expression regulation and control system is based on bCoro1a 3' UTR edited gene expression regulation and control system, and the expression level of bCoronin-1A is reduced in a targeted manner by inserting a specific bta-miR-27b target sequence into 3 'UTR, so that M.tb immune escape is inhibited, and the M.tb infection resistance of a host is improved.

The invention discloses a preparation method of a bionic magnetic nano-motor mixed and wrapped by a neutrophile granulocyte membrane and a stem cell exosome. The bionic magnetic nano-motor comprises the neutrophile granulocyte membrane, the stem cell exosome, a polylactic acid-glycolic acid copolymer and an anti-inflammatory drug. According to the method, a layer of polylactic acid-glycolic acid copolymer is wrapped outside magnetic ferroferric oxide nanoparticles and an anti-inflammatory drug by utilizing an ultrasonic emulsification method, and finally the polylactic acid-glycolic acid copolymer is wrapped by utilizing a neutrophile granulocyte membrane and a stem cell exosome, so that the bionic magnetic nano motor is obtained, and the motor has good biocompatibility. Meanwhile, the motor has an immune escape function and can resist phagocytosis of macrophages in blood. And under the control of an external alternating magnetic field, the medicine can accurately reach a spinal cord injury part, and the effects of inflammation inhibition and neuron recovery can be achieved under the mixed action of neutrophile granulocyte membranes, stem cell exosomes and anti-inflammatory drugs.

Disclosed are an aggregation-induced emission photosensitizer and a pharmaceutical composition constructed therefrom, a preparation method therefor and the use thereof. The aggregation-induced emission photosensitizer MTCN-3 has a great reactive oxygen species generation capacity and a photothermal effect, thus exerting the dual effect of inducing pyroptosis and ferroptosis in tumor cells. The aggregation-induced emission photosensitizer is also capable of exerting a synergistic photoimmunotherapeutic effect with an immune agonist Poly(I:C). A co-assembled pharmaceutical composition has a near-infrared aggregation-induced emission effect, exhibits good subcellular distribution, and has active targeting selectivity for tumor cells. The pharmaceutical composition eliminates tumors and prevents tumor metastasis by means of inhibiting immune evasion, and inhibits the growth of both primary and distal tumors, thereby exerting a systemic anti-tumor immune effect. The pharmaceutical composition exhibits high stability and low toxic side effects, and has broad prospects for clinical application.

We describe compositions of DNA donor molecules compatible with various gene insertion methods, offering key advantages in delivery, nuclear localization, and immune evasion. The modified DNA donor molecules are predominantly single-stranded but include short regions of double-stranded DNA to reconstruct enzyme binding sites, and can be combined with other methods to enhance donor recruitment to the cell nucleus.

The present disclosure provides methods of treating immune evasive cancers using surface functionalized particles alone or in combination with cancer therapeutics.

Provided herein are compositions for the prevention and treatment of genital herpes, comprising antigen binding agents to herpes simplex virus (HSV) glycoproteins, including those involved in virus entry and immune evasion, ribonucleic acids (RNAs) encoding these antigen binding agents, and methods of use thereof.

The invention relates to compositions including polynucleotides encoding polypeptides which have been chemically modified by replacing the uridines with 1-methyl-pseudouridine to improve one or more of the stability and / or clearance in tissues, receptor uptake and / or kinetics, cellular access by the compositions, engagement with translational machinery, mRNA half-life, translation efficiency, immune evasion, protein production capacity, secretion efficiency, accessibility to circulation, protein half-life and / or modulation of a cell's status, function, and / or activity.

The application discloses application of a PHD3 inhibitor in prevention and treatment of AIDS. Through immunological, biochemical and other multidisciplinary research means, the application analyzes the mechanism that a viral antisense protein ASP inhibits production of type I IFN to realize immune escape and establish latent infection in an HIV-1 infection process. Mechanically, after being expressed into a protein in a cell in the body, the ASP needs to undergo post-translational modification to exert its inhibiting effect, and after hydroxylation modification of a 47-position proline, the ASP can help to realize the ability of inhibiting the body immune response, and the post-translational modification depends on a host proline hydroxylase 3 (PHD3) to realize. Based on the mechanism-based research, it is found that a PHD3 inhibitor Molidustat offsets the hydroxylation of the ASP by PHD3, thereby blocking the immune evasion of HIV-1 and antagonizing infection, and showing a good development prospect of an AIDS treatment and prevention drug.

Invasive fungal disease (IFD) constitutes an increasing health concern due to growing numbers of patients at risk for opportunistic fungal infections. Among the fungi capable of inducing opportunistic infections the yeast Candida albicans is clinically the most important. Immune evasion proteins like the pH-regulated antigen 1 (Pra1) and the translation elongation factor 1 (Tef1), which are expressed on the fungal surface and are also secreted, are major drivers of pathogenicity. Therefore, novel monoclonal antibodies (mAb) binding these proteins have been developed. In an in vivo mouse model of high-dose septic C. albicans infection, therapeutic application of mAb against Pra1 reduced clinical symptoms of the disease. Prophylactically, mAb against Tef1 protected mice from clinical disease and prolonged survival. The mABs of the present invention may also be efficacious in patients at risk or with already established IFD.

The present disclosure provides, inter alia, techniques for identifying, characterizing, and / or monitoring variant sequences of specific reference infectious agents. The systems, methods, and architectures described herein provide, inter alia, visualization and decision support tools that can facilitate local current decision processes and improve epidemic measures, for example, in aspects such as resource allocation, policy formulation, and acceleration of customized vaccine development. The disclosure also provides tools for analyzing circulating variants to predict mutations that may increase immune escape of an infectious agent.

The present application belongs to the technical field of medicine and pharmacy, and in particular relates to an application of proto-prosolan in preparation of a Streptococcus suis type 2 capsule inhibitor. The present application discloses that proto-prosolan can significantly weaken the pathogenicity and immune escape ability of Streptococcus suis type 2 by inhibiting capsule synthesis, and then effectively plays an anti-infection role. Compared with vaccines, antibodies and phage enzymes and other highly limited anti-capsule strategies specific to serotypes, proto-prosolan, as an anti-toxicity inhibitor of Streptococcus suis type 2, has potential advantages such as broad spectrum, and has important scientific significance and application value for the research and development of new anti-drugs in the future. The proto-prosolan can be applied to the preparation of a Streptococcus suis type 2 capsule inhibitor and a drug for preventing and treating Streptococcus suis type 2 infection.

The present invention relates to: an immuno-oncology composition comprising an anti-MUC1 antibody or an antigen-binding fragment thereof that specifically binds to a polypeptide comprising the C-terminal extracellular domain of Mucin 1 (MUC1); and a use for inducing an immuno-oncology response in a subject by using same. The anti-MUC1 antibody or antigen-binding fragment thereof that specifically binds to a polypeptide comprising the C-terminal extracellular domain of MUC1 according to the present invention does not exhibit direct cytotoxicity to cancer cells, induces an increase in the activity of immune cells, and exhibits antibody-dependent cellular cytotoxicity (ADCC) by inhibiting immune evasion of cancer. Therefore, the anti-MUC1 antibody or antigen-binding fragment thereof can be used as various types of immuno-oncology agents, immuno-oncology adjuvants, or combination therapeutic agents for inducing an immune response in a subject and enhancing an anticancer effect.

The invention belongs to the technical field of biological medicine, and particularly relates to application of lncRNA in tuberculosis infection. According to the invention, THP-1 cells infected by M.tb are taken as a model, a plurality of lncRNAs related to M.tb infection are identified, and high expression of the lncRNA ENST00000608721 in tuberculosis infection is proved. By detecting the expression level, the tuberculosis infection state and the tuberculosis non-infection state can be effectively distinguished. Further research finds that the CFU in a silent lncRNA ENST00000608721 cell is obviously lower than that in a control group cell, which indicates that the removal capacity of macrophages to M.tb can be enhanced by knocking down the lncRNA ENST00000608721, and the bacteriostatic effect is exerted. It is shown that ENST00000608721 can be controlled and utilized by M.tb, and the ENST00000608721 serves as a negative regulation factor of host anti-tuberculosis infection immune response to help M.tb to achieve immune escape.