194 results about "TLR4" patented technology

The invention discloses a goat TLR4 gene knock-out vector and a construction method thereof. The construction method comprises the following steps: firstly, designing an sgRNA fragment of the TLR4 gene by adopting a CRISPR/cas9 system, synthesizing an sgRNA nucleotide sequence, constructing and simultaneously expressing the sgRNA and plasmid PYSY-sgRNA of Cas9 D10A, connecting and transforming to an Escherichia coli DH5 alpha competent cell, and verifying the transformant; and judging and proving by enzyme digestion and sequencing that the TLR4 gene knock-out vector is constructed correctly. The invention adopts the CRISPR/cas9 for constructing the vector, and provides a theoretical basis for subsequently acquiring a goat TLR4 gene deletion type alveolar epithelial cell system, and studying the immune response molecular mechanism of mycoplasma pneumonia infection.

The invention relates to an antigen and TLR agonist targeting co-loaded cationic phospholipid-polymer hybrid nanoparticle vaccine adjuvant, and a preparation method and an application thereof. A hydrophobic inner core is encapsulated with a TLR7 agonist, a phospholipid layer is encapsulated with a TLR4 agonist, an antigen is adsorbed by cationic phospholipids in the phospholipid layer, and ligation of a mannose ligand makes the vaccine adjuvant like a specific targeting antigen to have the dendritic cell presenting ability, so the DC cell intake and the maturation promoting effect are enhanced; and the antigen is protected by hybridized nanoparticles, the antigen uptake by DC cells is improved, immune response after antigen stimulation is significantly enhanced by the TLR agonist, and thecross-presentation of the antigen is significantly improved, so vaccine adjuvant has a strong potent T cell killing effect, can induce cytokine secretion, has a long-acting memory T cell response, andhas an excellent prevention effect on tumors.

With the current invention, we provide new methods of enhancing the T-cell stimulatory capacity of human dendritic cells (DCs) and their use in cancer vaccination. The method comprises the introduction of different molecular adjuvants to human DCs through transfection with at least two mRNA or DNA molecules encoding markers selected from the group of: CD40L, CD70, constitutively active TLR4 (caTLR4), IL-12p70, EL-selectin, CCR7 and/or 4-1 BBL; or in combination with inhibition of SOCS, A20, PD-L1 and/or STAT3 expression, for example through siRNA transfection. We could show a clear increase in the immunostimulatory capacity of DCs obtained in this way, enabling them to elicit an unexpectedly high T-cell immune response in vitro. Introduction of at least two of the above molecules, in combination with a tumor-specific antigen enables the DCs to elicit a significant host-mediated T-cell immune response in vivo against the tumor antigen and thus makes them very attractive in the manufacturing of anti-cancer vaccines.

We provide new methods of in vitro or in vivo enhancing the T-cell stimulatory capacity of human DCs and the use thereof in cancer vaccination. The method includes the introduction of different molecular adjuvants to human DCs by contacting or modifying them with mRNA or DNA molecule(s) encoding CD40L, and CD70 or constitutively active TLR4 (caTLR4).

This invention relates generally to antibodies that specifically bind Toll-like Receptor 4 (TLR-4), and to methods of using the anti-TLR4 antibodies as therapeutics and to methods of using the anti-TLR4 antibodies in methods of preventing transplant rejection and/or prolonging survival of transplanted biological material.

The present invention is a method for preventing or treating neuropathic pain. Using an agent to decrease the expression or activity of Toll-like receptor 4 (TLR4), behavioral hypersensitivity is attenuated thereby preventing or treating neuropathic pain in a subject in need of such treatment.

The present invention relates to biomarkers for colon cancers, specifically adenomas and adenocarcinomas in the GI tract. The inventors have discovered that the expression and/or overexpression of biomarkers such as CLDN1, GPR56, GRM8, LY6G6D, TLR4 and SLCO1B3 are indicative of adenomas and adenocarcinomas. A method of detecting colon cancer using targeted molecular imaging agents is also presented.

The present invention relates to the use of a TLR9 agonist and/or a TLR4 antagonist and/or a NOD2 agonist for treatment or prevention of disorders involving TLR4 activation, such as systemic sepsis and necrotizing enterocolitis.

The invention discloses a cell model having TLR4 immune response function and a method for constructing the cell model. The cell model and the method are characterized in that: three different bovine genes MD2, CD15 and TLR4 are connected and assembled to a vector by 2A sequence, the vector is delivered into a commercial cell line, and the constructed cell model has the function of LPS-mediated immune response. The cell model constructed in the invention and the construction method provide technical supports for the study of functions of the bovine TLR4 gene and the elucidation of the bovine TLR4 gene mechanism, therefore are valuable tool for studying bovine TLR4 gene functions.

Antisense oligonucleotide compounds, compositions and methods are provided for down regulating the expression of TLR4. The compositions comprise antisense oligonucleotides targeted to nucleic acids encoding TLR4. The compositions may also comprise antisense oligonucleotides targeted to nucleic acids encoding TLR4 in combination with other therapeutic and/or prophylactic compounds and/or compositions. Methods of using these compounds and compositions for down-regulating TLR4 expression and for prevention or treatment of diseases wherein modulation of TLR4 expression would be beneficial are provided.

An assay for Alzheimer's disease (AD) pathology in a living patient is disclosed wherein an amount of α7nAChR or TLR4 in a FLNA-captured protein complex or α7nAChR in an Aβ-captured protein complex or α7nAChR-FLNA, or TLR4-FLNA and/or α7nAChR-Aβ₄₂ complex present as a protein-protein complex in a sample is compared to the amount in a standard sample from a person free of AD pathology. An amount greater than in the standard sample indicates AD pathology. Also disclosed is an assay predictive of prognosis for treatment with a medicament in which the amount of an above protein or protein complex is compared to an amount in the presence of a medicament that binds to a FLNA pentapeptide and contains at least four pharmacophores of FIGS. 7-12. An amount of protein or protein complex determined in the presence of medicament that is less than the first amount indicates a favorable treatment prognosis.

The invention discloses application of hordenine in preparing a drug for treating hypophysoma, and relates to the technical field of biopharmacy. Specifically, in the application, the inventor finds that the hordenine can inhibit a TLR4/NF-kB/ MAPK signaling pathway, thereby being conductive to exerting the pharmaceutical effect on treating prolactinoma and adrenocorticotropic hormone adenoma, andsolving the problem of drug shortage for patients with the prolactinoma and the adrenocorticotropic hormone adenoma.

The invention provides bifidobacterium longum subsp. Longum KLDS K5 capable of preventing and relieving symptoms of colitis, and belongs to the technical field of microorganisms. The invention further provides a preparation method of the bifidobacterium longum subsp. Longum KLDS K5. Experiments show that the bifidobacterium longum provided by the invention can tolerate the human gastrointestinal environment, relieve weight loss in the ulcerative colitis disease period, improve colonic mucosa injury and reduce MPO activity, and inhibit oxidation-related factors through iNOS and COX-2 signal pathways so as to relieve inflammatory bowel diseases; nF-kappa B p65 nuclear transfer is inhibited through a TLR4/MyD88/NF-kappa B signal channel, the expression quantity of proinflammatory factors TNF-alpha, IL-1beta, IL-6 and IL-10 in colon is reduced, the transcriptional level of colon tight connection related proteins Claudin-1, ZO-1 and Occludin and mucoprotein MUC2 is up-regulated, the intestinal flora change after DSS induction can be improved in the genus level, and the richness and diversity of the intestinal flora are improved.