50 results about "CXCL10" patented technology

Disclosed is a method for diagnosing melanoma in a human subject, as well as a method for providing a prognosis to a human subject who is at risk of developing melanoma recurrence, and a method for determining the stage of melanoma in a human subject, comprising the step of determining the level of expression of phosphatase and actin regulator 1 (PHACTR1) gene, or fragments thereof, either alone or in combination with the level of expression of secreted integrin-binding phosphoprotein (SPP1), preferentially expressed antigen in melanoma (PRAME), growth differentiation factor 15 (GDF 15), and chemokine C-X-C motif ligand 10 (CXCL10) genes. Further, the invention relates to a diagnostic kit, comprising at least one substance for detection of the expression of PHACTR1, or fragments thereof, either alone or in combination with the detection of SPP1, PRAME, GDF15, and CXCL10, for the diagnosis or prognosis of melanoma.

Elevated blood levels of the chemokine CXCL10 polypeptide are associated with respiratory illnesses (e.g. SARS, influenza and community-acquired pneumonia) and are useful in diagnosis of patients. Methods are provided for diagnosis and treatment of patients suffering from respiratory illnesses. Methods are provided for identifying inhibitors of the CXCL10:CXCR3 axis, for use in treating patients suffering from respiratory illnesses.

A method scores a sample, by receiving a first dataset associated with a first sample obtained from a first subject, wherein said first dataset comprises quantitative data for at least two markers selected from the group consisting of: CCL22; CHI3L1; COMP; CRP; CSF1; CXCL10; EGF; ICAM1; ICAM3; ICTP; IL1B; IL2RA; IL6; IL6R; IL8; LEP; MMP1; MMP3; PYD; RETN; SAA1; THBD; TIMP1; TNFRSF11B; TNFRSF1A; TNFSF11; VCAM1; and VEGFA; and determining a first SDI score from said first dataset using an interpretation function, wherein the first SDI score provides a quantitative measure of the rate of change in joint structural damage in said first subject.

The application concerns means for determining the stage of hepatic tissue damage, in particular the hepatic fibrosis score of subjects infected with one or more hepatitis viruses. In particular, the means of the invention involve measuring the levels of expression of selected genes, said selected genes being:SPP1, andat least one gene from among A2M and VIM, andat least one gene from among IL8, CXCL10 and ENG, andoptionally, at least one gene from among the list of the following sixteen genes: IL6ST, p14ARF, MMP9, ANGPT2, CXCL11, MMP2, MMP7, S100A4, TIMP1, CHI3L1, COL1A1, CXCL1, CXCL6, IHH, IRF9 and MMP1.

Disclosed are peptides having activity against receptor CXCR3 are disclosed that exhibit activity in preventing the formation of new vessels and activity in mediating the dissociation of newly-formed vessels and resolving of wounds in the later stages of wound healing. Preferred peptides are derived from the α-helix portion IP-10 (CXCL10) or from IP-9 (CXCL11), are nontoxic, and smaller than naturally occurring peptides, making them useful in therapies against diseases or disease states marked by unwanted angiogenesis, including tumorogenic diseases such as cancers, and in healing of chronic wounds.

The invention discloses a marker for forecasting nasopharynx cancer transfer risk and an application thereof. The marker comprises ANXA1, CBR3, CLASP1, CXCL10, DCTN1, FNDC3B, LRIG1, FNDC3B, HDLBP, POLR2M, WSB2, WNK1, and YBX3. Molecular tags formed by 13 genetic expression formulas of the marker are capable of reflecting the biological specificity of a nasopharynx cancer patient, more accurately forecasting the transfer risk and prognosis of the nasopharynx cancer patient, and guiding clinical medication better. The forecasting efficiency to distance metastasis free survival is superior to thetraditional N-stage.

The present invention relates to the field of inflammatory bowel disease. More specifically, the present invention relates to the use of cytokines to detect, diagnose, and assess inflammatory bowel disease. In one embodiment, a method for diagnosing Crohn's Disease (CD) in a patient comprises the steps of (a) collecting a sample from the patient; (b) measuring the levels of at least one cytokine in the sample collected from the patient; and (c) comparing the levels of the at least one cytokine with predefined cytokine levels, wherein a correlation between the cytokine levels in the patient sample and predefined cytokine levels indicates that the patient has CD. In a specific embodiment, the at least one cytokine comprises Interferon (IFN)-gamma, Interleukin (IL)-1beta, IL-6, IL-8, IL-12, IL-17 and CXCL10.

Disclosed are peptides having activity against receptor CXCR3 are disclosed that exhibit activity in preventing the formation of new vessels and activity in mediating the dissociation of newly-formed vessels and resolving of wounds in the later stages of wound healing. Preferred peptides are derived from the α-helix portion IP-10 (CXCL10) or from IP-9 (CXCL11), are nontoxic, and smaller than naturally occurring peptides, making them useful in therapies against diseases or disease states marked by unwanted angiogenesis, including tumorogenic diseases such as cancers, and in healing of chronic wounds.

The invention discloses a kit for detection or assisted detection of tuberculous pleurisy. The kit comprises a device for detecting the expression amount of an immune factor, wherein the immune factor comprises (1) IL-6, IL-13, G-CSF, CCL1, CCL21, IP-10 (CXCL10), CCL8 (MCP-2), CXCL9 (MIG) and CXCL12 (SDF-1); or (2) at least one of IL-6, IL-13, G-CSF, CCL1, CCL21, IP-10 (CXCL10), CCL8 (MCP-2), CXCL9 (MIG) and CXCL12 (SDF-1). Experiments prove that a method for specifically identifying tuberculous pleurisy by taking hydrothorax as a detection object, utilizing a group of immunologic molecular marker, and adopting a multiple-factor microsphere detection technique is developed, and the purposes of improving the disease diagnosis accuracy rate, scientifically judging the state of illness and the like are realized by a multiple-factor combination manner.

The present invention aims at providing a medicament and a method for promoting replication of hepatocytes and a medicament and a method for ameliorating insulin resistance. An effective amount of a neutralizing agent for CXCL10 belonging to a subfamily of chemokines which are heparin-binding proteins is administered to the hepatocytes to promote the replication of the hepatocytes. As the neutralizing agent for CXCL10, a factor which is specifically bound to CXCL10 and inhibits an activity of CXCL10 or a factor which inhibits CXCL10 expression is suitably used. By administering the neutralizing agent to impaired hepatic tissue, it is possible to restore and regenerate the hepatic tissue. Meanwhile, by administering an effective amount of the neutralizing agent for CXCL10 to the hepatocytes, the insulin resistance in type II diabetes and metabolic syndrome is ameliorated.

The application relates to hepatic fibrosis, specifically to hepatic fibrosis that may appear in a patient infected with one or more hepatitis viruses and / or who is suffering from hepatitis, specifically chronic hepatitis. The application provides methods and means for determining the stage (or degree) of hepatic fibrosis of such a patient. Specifically, the methods and means of the application make it possible to determine whether or not the stage (or degree) of hepatic fibrosis of the patient has exceeded the stage of light fibrosis. The methods and means of the invention use a combination of biomarkers such as, in particular, the CXCL10 protein and hyaluronic acid (HA).

The invention provides a method of reducing ocular inflammation in an individual susceptible to ocular inflammation. The method involves administering to the individual an effective amount of a neutralizing agent specific for CXCL10. Also provided is a method for reducing spread of viral infection within ocular tissues of an individual susceptible to ocular viral infection, which involves administering to the individual an effective amount of a neutralizing agent specific for CXCL10. Further provided is a method of extending corneal graft survival following corneal transplantation in an individual, which involves administering to said individual an effective amount of a neutralizing agent specific for CXCL10. Additionally, the invention provides a method for identifying a compound for reducing ocular inflammation in an animal.

The current invention is related to the prevention and treatment of diseases including cancer, autoimmune disease, and infectious disease using CXC chemokines and the receptors to which they agonize. It has been found that certain chemokines, including CXCL4, CXCL9, CXCL10, and CXCL12 have various effects on toll-like receptors in various cell types and these can be utilized for disease treatment and prevention.

Elevated blood levels of the chemokine CXCL10 polypeptide are associated with respiratory illnesses (e.g. SARS, influenza and community-acquired pneumonia) and are useful in diagnosis of patients. Methods are provided for diagnosis and treatment of patients suffering from respiratory illnesses. Methods are provided for identifying inhibitors of the CXCL10:CXCR3 axis, for use in treating patients suffering from respiratory illnesses.

The invention belongs to the fields of biotechnology and medicine, and relates to an inhibitor capable of inhibiting the excessive proliferation of keratinocytes, an inhibitor composition, and applications of the inhibitor. The inhibitor taking triptolide, triptonide or tripterine as the representative can inhibit the excessive proliferation of the keratinocytes, specifically, the expression levels of STAT1 and p-STAT1 can be inhibited, then the expression level of miR-17-92mRNA is down-regulated, then, miR-17-92 target gene CDKN2B is regulated, the secretion levels of inflammatory factors CXCL1, CXCL10, CXCL16 and IL-6 in cells are inhibited, and finally, the cell cycle progression and immune function abnormity are inhibited; triptolide, tripterine and triptonide can effectively inhibit the proliferation of the keratinocytes, and the effective doses respectively achieve 60nM, 100nM and 80nM.

The invention relates to a reagent kit for the early warning and the diagnosis of severe hepatitis and hepatic failure and a preparation method thereof, which belong to the medical detection reagent. The reagent kit comprises an enzyme-linked immunosorbnent assay (ELISA) plate which is coated with a CXC chemokine ligand-10 (CXCL10)-resistant monoclonal antibody. The ELISA plate is prepared through the following steps that: (1) the CXCL10 monoclonal antibody is diluted by acetate buffer solution with the pH value of 4.6 until the concentration of the CXCL10 monoclonal antibody is 2 micrograms per milliliter; (2) the CXCL10 monoclonal antibody solution is filled into reaction holes of the blank chemical luminous ELISA plate to be statically placed for 12 hours at the temperature of 4 DEG C; (3) liquid inside the reaction holes is removed, and each reaction hole is adequately washed by washing liquor and is dried; and (4) the ELISA plate is sealed and then is dried. The reagent kit has the advantages that the sensitivity and the accuracy are high, the repeatability is good, the minimum detection limit can be 0.1pg / mL, the variation coefficient range is 6.5%-13.1%, and early warning and diagnosis can be provided for the severe hepatitis and the hepatic failure so as to provide sufficient time for doctors and patients to take reasonable prevention and treatment measures.

A method for inducing a protective immune response is disclosed, the method utilizing a composition comprising a CXCR3-binding chemokine such as CXCL10 (IP-10) administered in conjunction with a protein, peptide, polynucleotide, or other target antigen.

The present invention relates to a TNF-alpha (tumor necrosis factor-alpha) / CXCL-10 (C-X-C motif chemokine 10) double targeting antibody based on the IgG format. Specifically, it was verified that an antibody, in which scFv having a heavy chain variable region and a light chain variable region of the CXCL10 specific antibody binds to the C-terminus of the heavy chain variable region of the TNF-alpha specific antibody, is a bispecific antibody that effectively binds to both TNF- alpha and CXCL10, and thus the antibody can be useful as a double targeting antibody capable of identifying TNF- alpha / CXCL10. A composition of the present invention comprises a TNF- alpha / CXCL-10 double targeting antibody which effectively binds to both TNF- alpha and CXCL10. The double targeting antibody of the present invention has excellent TNF- alpha inhibitory activity and osteoclast differentiation inhibitory activity compared with the TNF- alpha or CXCL10 single targeting antibody. The composition of the present invention can be used in preventing or treating immunological disease.

The invention relates to a detection method of G-201A locus of predisposing gene CXCL10 relevant to progression of chronic hepatitis type B disease course. The method is a PCR-RFLP method (namely polymerase chain reaction-restriction fragment length polymorphism method). The invention further relates to a kit for detecting the predisposing locus and the application thereof. In addition, by linking the G-201A locus of gene with the occurrence risk of the progression of chronic hepatitis type B disease course, the invention determines CXCL10 as a novel predisposing gene of the progression of chronic hepatitis type B disease course and provides new genetic counseling content for people who are chronically infected with hepatitis type B about the early warning of disease severity.

The success of anti-tumor immune responses requires effector T cells to infiltrate solid tumors, a process guided by chemokines. Herein, we demonstrate that in vivo post-translational processing of chemokines by dipeptidylpeptidase 4 (DPP4, also known as CD26) limits lymphocyte migration to sites of inflammation and tumors. Inhibition of DPP4 enzymatic activity enhanced tumor rejection by preserving biologically active CXCL10, and increasing trafficking into the tumor by lymphocytes expressing the counter-receptor CXCR3. Furthermore, DPP4 inhibition improved adjuvant-based immunotherapy, adoptive T cell transfer and checkpoint blockade. These findings provide the first direct in vivo evidence for controlling lymphocyte trafficking through CXCL10 cleavage and support the use of DPP4 inhibitors for stabilizing the biologically active form of chemokines as a strategy to enhance tumor immunotherapy.

Cardiovascular tissue mRNA expression profiles in monkeys treated with coxibs was analyzed. Genomic data indicated that the animals showing vasculitis exhibit a specific mRNA expression pattern. The pattern includes gene expression changes involved in blood and endothelial cell (EC) activation, interaction of blood cells with EC, activation of INFγ pathway, and release of pro-inflammatory cytokines and chemo-attractants. These results provide direct evidence of minimal vasculitis together with corresponding genomic signature and peripheral biomarkers for minimal vasculatis. These results also suggest that treatment might triggers / aggravate a clinically latent cardiovascular disorder in the context of an endothelium tropic viral infection and / or an autoimmune vascular disorder. The histopathological examination revealed marginal vascular changes consistent with the genomic findings. Measurement of soluble proteins present in serum and plasma using a multiplex assay were in line with the genomic results, showing the increased level of INFγ inducible proteins, increased expression of CXCL10 chemokine was confirmed by an ELISA both in serum and plasma. Use of these peripheral biomarkers allows a safe usage of cox-2 inhibitory compounds in clinics and selection of cox-2 inhibitory follow-up compounds with no cardiovascular toxicity. These data together with biochemical and histopathological findings suggest that the specific cox2 inhibitor may exaggerate host immune response during some specific viral infections with endothelial tropism, or subjacent vascular autoimmune disorders.

The invention discloses application of LINC01503 serving as therapeutic target to preparation of medicines for treatment of pediatric asthma. According to comparison between LINC01503 and a normal control, expression of LINC01503 in asthma patients is increased remarkably; LINC01503 in M1 macrophage is evidently down-regulated while LINC01503 in M2 macrophage is evidently up-regulated. According to siRNA knock-down experiments, LINC01503 promotes activation of M1 macrophage and realizes expression up-regulation of M1 marker genes such as IL-6, TNF-alpha and CXCL10; LINC01503 inhibits activation of M2 macrophage and realizes expression down-regulation of M2 marker genes such as CD206 and CD209. By Western blot, the fact that LINC01503 has influences on macrophage activation mainly through promotion of EPK phosphorylation, so that pediatric asthma can be effectively treated by inhibition of LINC01503 and downstream signal routing thereof.

The invention discloses a construction method of animal and cell models for improving rosacea inflammation by artemisinin, and relates to the technical field of skin disease medicaments, in particularto a construction method of animal and cell models for improving rosacea inflammation by artemisinin. The method comprises the following steps of: (1) constructing an animal model for improving rosacea inflammation phenotype by artemisinin; and (2) constructing a cell model for improving rosacea inflammatory phenotype by artemisinin. The invention has the advantages that a potential new drug (artemisinin) for treating rosacea is discovered; the pathogenesis of the rosacea is explored; it is found that artemisinin can obviously improve LL37-induced rosacea-like inflammatory mouse skin lesion erythema, histopathological changes and increase of IL-1 beta, IL-6, TNF alpha and TLR2; meanwhile, artemisinin can reduce infiltration of skin lesion CD4 + T cells, macrophages and neutrophils and inhibit expression of immune cell related chemokines (CXCL10, CCL20, CCL2 and CXCL2) in skin lesion.

The present invention relates to a method for treating vitiligo in a subject in need thereof comprising a step of administering to said subject a therapeutically effective amount of an antagonist of CXCR3B. Inventors have demonstrated that in skin and blood samples obtained from vitiligo subjects the population of the innate immune system is increased (NK and ILC1 cells). For the first time, inventors have shown that melanocytes express CXCR3, more 10 particularly CXCR3B (RNA and protein expressions). They have shown that the expression of CXCR3B on melanocytes is responsible of the destruction of melanocytes upon local stimulation with CXCL10. Inventors have demonstrated for the first time that siRNA of CXCR3B or CXCR3B antagonist prevent the CXL10-induced apoptosis of melanocytes. This initial apoptosis of melanocyte triggers the secondary adaptive immunity against melanocytes 15 that further destroys the remaining melanocytes. Accordingly, the inventors have found a new target to prevent and treat vitiligo.

The present invention pertains to compounds and their combination for use in the prevention or therapy of a subject suffering from an autoimmune disease such as diabetes type 1. Provided are antagonists of T-cells that are used in combination with antagonists of the cytokine CXCL10, sequentially or concomitantly, in a subject suffering from an autoimmune disease, in particular diabetes type 1.

The invention discloses an application of a PAX6 gene or an expression product thereof to preparation of medicines for restraining fibrosis. Experiment confirms that the PAX6 can restrain a fibrosis promotion factor TGF beta and promote fibrosis restraining factors IL1R2 and CXCL10, so that the effects of protecting the heart and restraining fibrosis can be achieved, and the PAX6 is a potential bran-new important target point for treating heart fibrosis so as to prevent heart failure in the heart.