42 results about "TLR5" patented technology

The invention provides an immunomodulatory flagellin peptide having substantially the same amino acid sequence GALNEINNNLQRVRELAVQSANSTNSQSDLDSIQAEITQ (SEQ ID NO:44), or a modification thereof, and having toll like receptor 5 (TLR5) binding. The immunomodulatory flagellin peptide also can have substantially the same amino acid sequence TQFSGVKVLAQDNTLTIQVGANDGETIDIDLKQINS QTLGLDTL (SEQ ID NO:45); EGALNEINNNLQRVRELAVQSANSTNSQSDLDSIQAEITQRLNEIDRVNG (SEQ ID NO:46) or MAQVINTNSLSLLTQNNLNKSQSALGTAIERLSSGLRINSAKDDAAGQAIANF TANIKGLTQASRNANDGISIAQTTEGALNEINNNLQRVRELAVQS (SEQ ID NO:47), or a modification thereof. Also provided is an immunomodulatory flagellin peptide having substantially the same amino acid sequence LQKIDAALAQVDTLRSDLGAVQNRFNSAITNL (SEQ ID NO:48), or a modification thereof, and having toll like receptor 5 (TLR5) binding. The immunomodulatory flagellin peptide also can have substantially the same amino acid sequence TLRSDLGAVQNRFNSAITNLGNTVNNLSS (SEQ ID NO:49) or EQAAKTTENPLQKIDAALAQVDTLRSDLGAVQNRFNSAITNLGNTVNNLSS (SEQ ID NO:50), or a modification thereof. Further provided is an immunomodulatory flagellin peptide having substantially the same amino acid sequence GALNEINNNLQRVRELAVQSANSTNSQSDLDSIQAE ITQ (SEQ ID NO:44) and substantially the same amino acid sequence LQKIDAALAQVDTLRSDLGAVQNRFNSAITNL (SEQ ID NO:48), or a modification thereof, and having toll like receptor 5 (TLR5) binding. Methods of using immunomodulatory flagellin peptides additionally are provided.

It has long been known that eosinopenia is observed during acute bacterial infection yet the mechanism remains undefined. Herein, we investigated the consequence of exposure to microbial products, specfically bacterial lipopolysaccharide (LPS), on eosinophil production. We demonstrate that developing murine eosinophils transiently express mRNA for six Toll-like receptors (TLR5) with highest expression of TLR2 and TLR4 throughout eosinophil development and nearly undetectable levels on mature eosinophils. LPS stimulation of eosinophil progenitors ex vivo markedly inhibited IL-5- mediated cellular proliferation and expansion Further LPS adrninistratwn in vivo reduced numbers of eosinophil progenitors in the bone marrow and blood in mice. Notably, LPS effectively reduced eosinophilia even in hypereosinophilic mice induced by the IL-S transgene. Taken together, these findings identify a mechanistic explanation for eosinopenia following bacterial infections and a novel therapeutic strategy for depleting eosinophil progenitors and inhibiting peripheral eosinophilia in eosinophil associated diseases.

Disclosed herein are flagellin mutants having an enhanced activity of stimulating the toll-like receptor-5 (hereinafter referred to as ''TLR5''). More specifically, disclosed are flagellin mutants, prepared by point-mutating some of the amino acids of a TRL5 agonist flagellin so as to enhance the TRL-stimulating activity of the flagellin.

The present invention relates to methods and pharmaceutical compositions for the treatment of respiratory tract infections. More particularly, the present invention relates to a TLR5 agonist for use in a method for treating a respiratory tract infection.

Disclosed is a method for rapidly amplifying CD8+ T cells and functional cell subpopulations thereof in vitro. A TLR1/2 agonist, a TLR2/6 agonist and a TLR5 agonist or a combination of above agonists is added to a conventional culture system for in-vitro amplification of CD8+ T cells. Recombinant cytokines IL-2, IL-7 and IL-15 as well as magnetic beads coated with an anti-human CD3 antibody and an anti-human CD28 antibody can be further added to the culture system for continuous co-stimulation.

The invention belongs to the technical field of biology and in particular relates to an NF-kB dual-luciferase reporter cell for stably expressing swine TLR5 receptor genes and a construction method thereof. A cell line refers to HEK293-NF-kB cells in which the swine TLR5 receptor genes are transferred, and the HEK293-NF-kB cells refer to HEK293 cells in which NF-kB firefly luciferase and renilla luciferase are transferred. The invention provides the stable cell line used in detection for researching pTLR5 activated downstream NF-kB promoter report genes. The invention also provides a biological material for performing high-throughput screening on differentially expressed genes in stable cells in quiesced and activated states in an RNA-Seq technology, and lays a foundation and platform forfurther researching species specificity of TLR5.

Biomarkers useful for diagnosing and assessing the extent of coronary artery disease (CAD) are provided, along with kits for measuring their expression. The invention also provides predictive models, based on the biomarkers, as well as computer systems, and software embodiments of the models for scoring and optionally classifying samples. In a preferred embodiment, the biomarkers are organized into clustered groups. The expression level of the biomarkers within a group are highly correlated to each other in normal and disease states. Expression values of genes chosen from each of two, three, four or five of the clustered gene groups, A, B, C, D, E may be used. Alternatively, expression values of genes chosen from the groups are combined into a metagene. Preferred biomarkers include S100A12, S100A8, S100A9, BCL2A1, and F5 (group A); XK, P62, and FECH (group B); TUBB2 (group C); IFNG, PDGFB, VSIG4, and TNF (group D); CSF3R, TLR5, CD46, and NCF1 (group E); S100A12, S100A9, BCL2A1, TXN and CSTA (group I); OLIG1, OLIG2, ADORA3, CLC, and SLC29A1 (group II); and CBS and ARG1 (group IV).

Antisense oligonucleotide compounds, compositions and methods are provided for down regulating the expression of TLR5. The compositions comprise antisense oligonucleotides targeted to nucleic acids encoding TLR5. The compositions may also comprise antisense oligonucleotides targeted to nucleic acids encoding TLR5 in combination with other therapeutic and/or prophylactic compounds and/or compositions. Methods of using these compounds and compositions for down-regulating TLR5 expression and for prevention or treatment of diseases wherein modulation of TLR5 expression would be beneficial are provided.

The invention relates to a new ionizing radiation damage resistance function of polyethyleneimine (PEI) compounds, and its application. The PEI mainly has two structures comprising a linear structure (the molecular formula is (C2H5N)x) and a branched structure (the molecular formula is (C2H5N)x[-N(C2H6N)C2H4-]y), wherein each of x and y is an integer not lower than 1. The PEI can specifically activate a cell TLR5 acceptor mediated NF-kappaB signal channel. Results of experiment researches show that the PEI is weakly toxic to cells and animals, can substantially activate the cell TLR5 acceptor mediated NF-kappaB signal channel and display a dosage dependency, and can substantially reduce the mortality of ionizing radiation damaged mice and prolong the animal survival time. The new ionizing radiation damage resistance function of the PEI can be used for researching medicines for preventing and treating ionizing radiation damages and damages caused by radiotherapy.

In vitro method and kit for prognosis or prediction of the response of rheumatoid patients to treatment with TNF-α factor blocking agents, which comprises determining, in a blood sample from said patients, the expression level of at least one of the eight genes selected from the group: HLA-DRB3, EAT2, GNLY, CAMP, SLC2A3, IL2RB, MXD4 and TLR5 or combinations thereof and comparing said expression level to the expression values obtained from responsive and non-responsive patients who showed responsiveness to the treatment and those who showed non-responsiveness thereto.

The present invention relates, in part, to compositions and methods for enhancement of an immune response and for increased vaccine efficacy by stimulation of the TLR5 receptor, for example, with a recombinant TLR5 agonist (e.g., a flagellin-based agent or variant thereof).

Disclosed herein are flagellin mutants having an enhanced activity of stimulating the toll-like receptor-5 (hereinafter referred to as “TLR5”). More specifically, disclosed are flagellin mutants, prepared by point-mutating some of the amino acids of a TRL5 agonist flagellin so as to enhance the TRL-stimulating activity of the flagellin.

Compositions and method of increasing levels of apoA1 and/HDL in a subject in need thereof are provided. The compositions include one or more TLR5 agonists in a pharmaceutically acceptable carrier in an effective amount to increase the level of apoA1 and/or HDL in a subject. In a preferred embodiment, the composition is an oral formulation of the one or more TLR5 agonists. The disclosed methods include administering compositions containing the one or more TLR5 agonists to a subject in need thereof, in an effective amount to increase levels of apoA1 and/or HDL in the subject. In one preferred embodiment, the subject is at risk of developing atherosclerosis and/or coronary heart disease. In some embodiments, the subject is diagnosed as having atherosclerosis. The disclosed compositions can also be administered to subjects presenting with hyperlipidemia or hypercholesterolemia.