41 results about "CCL5" patented technology

Biomarker-based treatment, monitoring, and diagnostic methods for IL-17 dependent conditions, including hidradenitis suppurativa, are disclosed. The biomarkers may be selected from IL6, PLA2G2A, IL19, P13, CST7, IL17A, IL17F, GH1, MZB1, IL1B, IFNG, TNC, CXCL9, SLAMF7, VEGFA, IL17C, SLAMF1, SDC1, OSM, LBP, REG3A, CD79B, COL4A1, CLEC4D, VWF, IL5RA, CSF3, TGFA, IL2RA, ITIH3, FCAR, CCL23, NRCAM, RETN, SERPINA11, CLEC4G, CSF1, HGF, CRELD2, EFEMP1, LTBR, NME3, CKAP4, CD276, SPON2, GGH, TIMP1, LY9, MCFD2, TCN2, QPCT, HYOU1, TNSFSF13B, CCL2, CCL3, CCL4, CCL5, CCL7, CCL20, CXCL1, CXCL8, PDFGA, CXCR2, CCR6, CXCL13, PCDH1, BOC, MEPE, ADAM 23, THOP1, IL1RL2, RCOR1, EDAR, and combinations thereof. Kits for measuring the biomarkers, diagnosing and treating IL-17-dependent conditions, and identifying super-responders are also disclosed.

The disclosure provides methods and uses of CCL5 variants for modulating GPR75 signaling in a cell or subject, treating a GPR75-related disease or disorder in a subject, treating obesity, hypertension, metabolic syndrome, metabolic dysfunction-associated steatohepatitis, and / or diabetes in a subject, and inducing weight loss and / or preventing weight gain in a subject, wherein the CCL5 variant comprises a variant N-terminal portion and a C-terminal portion with at least 70% identity to the corresponding portion of wild type CCL5.

Biomarker-based treatment, monitoring, and diagnostic methods for IL-17 dependent conditions, including hidradenitis suppurativa, are disclosed. The biomarkers may be selected from IL6, PLA2G2A, IL19, PI3, CST7, IL17A, IL17F, GH1, MZB1, IL1B, IFNG, TNC, CXCL9, SLAMF7, VEGFA, IL17C, SLAMF1, SDC1, OSM, LBP, REG3A, CD79B, COL4A1, CLEC4D, VWF, IL5RA, CSF3, TGFA, IL2RA, ITIH3, FCAR, CCL23, NRCAM, RETN, SERPINA11, CLEC4G, CSF1, HGF, CRELD2, EFEMP1, LTBR, NME3, CKAP4, CD276, SPON2, GGH, TIMP1, LY9, MCFD2, TCN2, QPCT, HYOU1, TNSFSF13B, CCL2, CCL3, CCL4, CCL5, CCL7, CCL20, CXCL1, CXCL8, PDFGA, CXCR2, CCR6, CXCL13, PCDH1, BOC, MEPE, ADAM23, THOP1, IL1RL2, RCOR1, EDAR, and combinations thereof. Kits for measuring the biomarkers, diagnosing and treating IL-17-dependent conditions, and identifying super-responders are also disclosed.

The invention discloses an application of a substance for detecting a marker group. The application comprises one or more of the following applications: A1) an application in preparation of a product for predicting sensitivity of bicitinib combined with narrow-spectrum medium-wave ultraviolet rays in treatment of leucoderma, and A2) an application in preparation of a product for predicting sensitivity of bicitinib combined with narrow-spectrum medium-wave ultraviolet rays in treatment of leucoderma; a2) is applied to preparation of a product for screening sensitivity of bicitinib combined with narrow-spectrum medium-wave ultraviolet rays in treatment of leucoderma; a3) in preparation of a product for evaluating sensitivity of bicitinib combined with narrow-spectrum medium-wave ultraviolet rays in treatment of leucoderma; the marker group is composed of CCL5, FGL1, EZR and GAPDH (glyceraldehyde-phosphate dehydrogenase). The invention screens and verifies the plasma and urine biomarker group capable of predicting the sensitivity of treating leucoderma by combining baricitinib with narrow-spectrum medium-wave ultraviolet rays of a subject through ELISA (Enzyme-Linked Immunosorbent Assay), and the plasma and urine biomarker group provided by the invention has higher prediction accuracy, sensitivity and specificity; the individualized treatment of vitiligo can be improved, and good clinical application and popularization prospects are achieved.

The present invention provides a method for the diagnosis in vitro of colon cancer in a subject that comprises (i) determining in a sample isolated from the subject the expression level of at least one gene selected from the list consisting of LNC-TBP-2, CCL5, DENND2B, LRRC52-AS1, and RNF31, (ii) calculating a variable S, wherein S= A +B + C – D – E, and wherein: A is the expression level of gene LNC-TBP-2 when the expression level of gene LNC-TBP-2 is determined in step (i), or is 0 when the expression level of gene LNC-TBP-2 is not determined in step (i); B is the expression level of gene CCL5 when the expression level of gene CCL5 is determined in step (i), or is 0 when the expression level of gene CCL5 is not determined in step (i); C is the expression level of gene DENND2B when the expression level of gene DENND2B is determined in step (i), or is 0 when the expression level of gene DENND2B is not determined in step (i); D is the expression level of gene LRRC52-AS1 when the expression level of gene LRRC52-AS1 is determined in step (i), or 0 when the expression level of gene LRRC52-AS1 is not determined in step (i); and E is the expression level of gene RNF31 when the expression level of gene RNF31 is determined in step (i), or is 0 when the expression level of gene RNF31 is not determined in step (i); and (iii) diagnosing the subject as having colon cancer if S calculated in step (ii) is equal or lower than a corresponding reference value. The present invention also provides the use of LNC-TBP-2, CCL5, DENND2B, LRRC52-AS1, and RNF31 as biomarkers of CRC.

The invention belongs to the field of biological pharmacy, and relates to an anti-tumor nano-drug, in particular to a tumor-targeted anti-tumor nano-drug HPCR as well as a preparation method and application thereof. An immune checkpoint inhibitor anti-PD-L1, a chemotactic factor CCL5 and rutin with an ACE2 activation effect are respectively grafted to HA through a chemical synthesis method to synthesize HA-anti-PD-L1, HA-CCL5 and HA-RT, then the HA-anti-PD-L1, HA-CCL5 and HA-RT are synthesized into the anti-tumor nano-drug HPCR through a film hydration method, and in-vivo experiments prove that the drug has an excellent anti-tumor effect; the medicine has good T cell activation effect, T cell recruitment effect, tumor matrix elimination, T cell infiltration increase and medicine permeation effects, and provides a new method and a new thought for tumor treatment.

The invention relates to the technical field of biology, and provides a predictive biomarker for treating adverse reactions of tumor patients by using CCL5 as an immune checkpoint inhibitor and application of the predictive biomarker, and the predictive biomarker is the dynamic change of the CCL5 relative to a baseline proportion. The detection kit is used for detecting the proportion of CCL5. The dynamic change refers to the change of the CCL5 proportion before and after the immune checkpoint inhibitor is used; if the dynamic change is greater than or equal to 50% or continuously increased, the immune checkpoint inhibitor causes adverse reaction when treating the tumor patient. According to the method, high-risk patients can be identified through peripheral blood detection before irAEs have obvious clinical manifestations, so that a basis for advanced intervention is provided for clinicians, and the occurrence probability of serious adverse events is reduced.

The present disclosure relates to a lipid-like nanoparticle encapsulating a C—C motif chemokine ligand 5 (CCL5) mRNA and methods of use thereof.

This disclosure provides a method for treating a cancer patient comprising administering to the patient a therapeutically effective amount of an anti-PD-1 antagonist, for example, an anti-PD-1 or anti-PD-L1 antibody, in combination with an indolamine 2,3-dioxygenase inhibitor, wherein the patient is identified as exhibiting a combined biomarker comprising (a) a high IFNγ inflammatory signature score and (b) a low tryptophan 2,3-dioxygenase 2 (TDO2) gene expression score. The high IFNγ inflammatory signature score is determined by measuring the expression of a panel of IFNγ-related inflammatory genes in a cancer sample obtained from the patient, wherein the gene panel comprises, for example, IFNγ, CXCL10, CXCL9, HLA-DRA, IDO1, and STAT1. In some respects, the gene panel also includes CCR5, CXCL11, GZMA, and PRF1.In some aspects, the genetic panel comprises CXCR6, TIGIT, PD-L1, PD-L2, LAG3, NKG7, PSMB10, CMKLR1, CD8A, IDO1, CCL5, CXCL9, HLA.DQA1, CD276, HLA.DRB1, STAT1, HLA.E and TDO2.

The invention discloses application of a targeted Nup85 inhibitor in preparation of a medicine for preventing or treating hepatocellular carcinoma, and relates to the technical field of biological medicine and tumor immunotherapy. The invention provides an application of a targeted Nup85 inhibitor in preparation of a medicine for preventing or treating hepatocellular carcinoma. The inhibitor prevents and / or treats hepatocellular carcinoma by enhancing CD8 + T cell functions, enhancement of the CD8 + T cell functions is realized by regulating STAT1 / CCL5 / CXCL10 pathways, and Nup85 reduces expression of CCL5 and CXCL10 by inhibiting nuclear translocation of phosphorylated STAT1, so that infiltration and activation of CD8 + T cells are inhibited. The invention discloses an immune escape mechanism that Nup85 inhibits CD8 + T cell infiltration by inhibiting p-STAT1 nuclear translocation and down-regulating CCL5 / CXCL10 expression in liver cancer for the first time, provides a new liver cancer immunotherapy target, and broadens the application of nucleopore protein in tumor immunotherapy; the target Nup85 inhibitor can be obtained through a conventional means, a new clinical application direction of the target Nup85 inhibitor is defined, and the target Nup85 inhibitor has good clinical transformation and development prospects.

The disclosure provides a method for treating a subject afflicted with a cancer comprising administering to the subject a therapeutically effective amount of an anti-PD-1 antagonist, e.g., an anti-PD-1 or anti-PD-L1 antibody, in combination with an indoleamine 2,3-dioxygenase inhibitor, wherein the subject is identified as exhibiting a combined biomarker comprising (a) a high IFNγ inflammatory signature score and (b) a low tryptophan 2,3-dioxygenase 2 (TDO2) gene expression score. The high IFNγ inflammatory signature score is determined by measuring the expression of a panel of IFNγ related inflammatory genes in a cancer sample obtained from the subject, wherein the gene panel comprises, e.g., IFNγ, CXCL10, CXCL9, HLA-DRA, IDO1, and STAT1. In some aspects, the gene panel further comprises CCR5, CXCL11, GZMA, and PRF1. In some aspects, the gene panel comprises CXCR6, TIGIT, PD-L1, PD-L2, LAG3, NKG7, PSMB10, CMKLR1, CD8A, IDO1, CCL5, CXCL9, HLA.DQA1, CD276, HLA.DRB1, STAT1, HLA.E, and TDO2.

The invention provides an establishment method and application of a Zika virus infectious animal model, and belongs to the technical field of biology. According to the invention, ZIKV is inoculated to Toll-like receptor-deleted animals, such that the ZIKV challenging animal model is obtained. After the animal is inoculated with ZIKV, obvious ZIKV load can be detected in blood, liver, spleen, reproductive organ and brain tissue of the animal, moreover, the spleen is obviously swollen, the liver tissue has punctiform necrotic lesion, the splenosome is obviously reduced, and the mRNA level of inflammation related indexes Ccl5, Cxcl1, Isg15 and Isg56 is obviously up-regulated, which indicates that the ZIKV challenge model disclosed by the invention is successfully constructed; the method can be used in related researches such as ZIKV infection mechanism, vaccine research and development, anti-ZIKV drug research and development and the like.

The invention relates to the technical field of genetic engineering and pharmaceutical preparations, in particular to a hydrogel drug delivery system carrying recombinant protein for cancer treatment and a preparation method of the hydrogel drug delivery system, the hydrogel drug delivery system comprises recombinant plasmids, the recombinant plasmids are protein pcDNA3.4-PD1-ECD-CCL5 with an amino acid sequence, and the amino acid sequence of the protein is Pab-CCL5. According to the present invention, the recombinant plasmid can express the fusion protein of PD1-ECD-IgG1 and CCL5-IgG1, and the recombinant protein Pab-CCL5 prepared by using the recombinant plasmid has good anti-tumor effect, can change the immune state of the tumor microenvironment, and can reshape the tumor microenvironment; immune cells expressing CCL5 receptors are recruited, and the anti-tumor immune response of the body is improved; the compound kills tumor cells through multiple mechanisms including innate immunity and adaptive immunity, is a potential candidate drug for treating prostate cancer, breast cancer and PD-L1 expression cancer, and is free of cytotoxicity.

The invention relates to a biomarker for Parkinson's disease diagnosis and application thereof, and belongs to the technical field of biological detection. The biomarkers comprise one or more of NDUFC1 (Non-Dulbecco Fluorescent Receptor 1), CHGA (Chrysanthemum Glycolic Acid), CCL5 and ST3GAL6. The biomarker can play an important role in mechanism research of Parkinson's disease. According to the invention, a group of Parkinson's disease diagnosis biomarkers are found in neuron-derived exosomes and planetary glial cell-derived exosomes of a Parkinson's disease clinical queue by combining machine learning with a proteomics method, and the AUC value reaches 0.967.

The present disclosure provides a clinically applicable method to re-balance production of hematopoietic cells in a mammal, including without limitation an aged mammal, by disrupting the CCL5-CCR5 axis.

The application belongs to the technical field of biological medicine, and particularly relates to a binding molecule targeting CCL5 and application of the binding molecule in combination with drugs in treatment of Th2-type inflammation related diseases. The application discloses use of a binding molecule targeting CCL5 or a pharmaceutical composition comprising the binding molecule in preparation of a product having one or more of the following functions: 1) prevention and / or treatment of Th2-type inflammation related diseases; 2) reduction of skin lesion tissue thickness; 3) reduction of clinical score of atopic dermatitis; 4) reduction of scratching behavior; 5) reduction of tissue damage; 6) alleviation of inflammatory reaction and inhibition of expression of inflammatory factors; and 7) reduction of inflammatory cell infiltration. The binding molecule targeting CCL5 or the pharmaceutical composition comprising the binding molecule has important value in prevention and treatment of immune inflammatory diseases such as atopic dermatitis, allergic rhinitis, asthma, food allergy or drug allergy.

The present disclosure relates to a composition for promoting the activation of bone marrow-derived stem cells, including C-C motif chemokine ligand 5 (CCL5), wherein, when CCL5 is administered together with growth-related oncogene beta (GROβ) and AMD3100, it not only increases the migration of hematopoietic stem cells from bone marrow to peripheral blood, but also enhances the engraftment efficiency when the hematopoietic stem cells are transplanted into recipients.

Biomarker-based treatment, monitoring, and diagnostic methods for IL-17 dependent conditions, including hidradenitis suppurativa, are disclosed. The biomarkers may be selected from IL6, PLA2G2A, IL19, PI3, CST7, IL17A, IL17F, GH1, MZB1, IL1B, IFNG, TNC, CXCL9, SLAMF7, VEGFA, IL17C, SLAMF1, SDC1, OSM, LBP, REG3A, CD79B, COL4A1, CLEC4D, VWF, IL5RA, CSF3, TGFA, IL2RA, ITIH3, FCAR, CCL23, NRCAM, RETN, SERPINA11, CLEC4G, CSF1, HGF, CRELD2, EFEMP1, LTBR, NME3, CKAP4, CD276, SPON2, GGH, TIMP1, LY9, MCFD2, TCN2, QPCT, HYOU1, TNSFSF13B, CCL2, CCL3, CCL4, CCL5, CCL7, CCL20, CXCL1, CXCL8, PDFGA, CXCR2, CCR6, CXCL13, PCDH1, BOC, MEPE, ADAM 23, THOP1, IL1RL2, RCOR1, EDAR, and combinations thereof. Kits for measuring the biomarkers, diagnosing and treating IL-17-dependent conditions, and identifying super-responders are also disclosed.

The invention relates to a marker and a prediction model for predicting the shunt operation curative effect of an idiopathic normal pressure hydrocephalus patient and application of the marker and the prediction model, and belongs to the technical field of biological detection. The marker combination disclosed by the invention comprises genes IFN gamma, IL-1beta, IL-6, TNF-alpha, CCL3, CCL4, CCL5, CXCL16, GZMB and TGF beta. The marker combination provided by the invention is closely related to the prognosis effect of the iNPH, and a prediction model for the shunt operation curative effect of the patient with the idiopathic normal pressure hydrocephalus can be further constructed through the marker combination. The embodiment verifies that when the marker combination is used for predicting the shunt operation curative effect of the idiopathic normal pressure hydrocephalus patient, the sensitivity can reach 100.0%, and the specificity can reach 96.0%.

The invention belongs to the technical field of medicines, and discloses application of IRE1alpha protein or a coding gene thereof as a new target spot for treating hepatitis B virus. The invention reveals for the first time that IRE1alpha protein weakens the recruitment and function of HBV specific CD8 + T cells by promoting macrophages to be polarized to anti-inflammatory phenotypes and inhibiting secretion of chemotactic factors CCL5, and the IRE1alpha protein is a key host factor for maintaining immune tolerance. On the basis, the invention provides an application of a small-molecule inhibitor targeting IRE1alpha in resisting HBV, and provides a new molecular mechanism and a candidate drug for functional healing of HBV.

The invention provides a CCL5 and CXCL9 high-expression targeting EGFR (epidermal growth factor receptor) CART (chimeric antigen receptor T) cell as well as a preparation method and application thereof, a strain of targeting EGFR monoclonal antibody with relatively strong affinity is firstly obtained, and a strain of targeting EGFR CART cell with high-expression CCL5 and CXCL9 is obtained on the basis of the monoclonal antibody. The cell can recognize and combine EGFR protein highly expressed on the surface of a tumor cell by expressing scFv of EGFR, and transmits a signal to a T cell through an intracellular signal transduction region, so that the T cell is activated, the T cell is promoted to secrete cytokines, the cytokines can kill tumor cells highly expressing EGFR protein, the T cell can be continuously activated and proliferated, and the tumor cells with high expression of EGFR protein can be killed. Cytokines are continuously secreted, so that the effect of killing tumor cells is enhanced.

The invention belongs to the technical field of medicines, and particularly discloses application of a compound 84-B10 in preparation of myocardial protection medicines. In order to solve the problems that in the prior art, effective therapeutic drugs are lacked for myocardial injury caused by sepsis and chemotherapeutic drugs (cis-platinum and adriamycin), and an existing cardiac protective agent possibly interferes with the chemotherapeutic effect, 84-B10 is used for preparing the myocardial protective drug, and the 84-B10 is particularly suitable for patients suffering from cardiac function injury caused by sepsis or chemotherapeutic drugs. Experiments show that the medicine can significantly improve the cardiac ejection fraction and shortening rate, reduce the levels of serum lactic dehydrogenase (LDH) and creatine kinase isoenzyme (CK-MB), and inhibit the expression of chemotactic factors (CCL5 and CXCL1) and inflammatory factors (IL-6 and IL-17A) in cardiac muscle tissues. Meanwhile, the medicine does not interfere with the killing effect of adriamycin on tumor cells, and the curative effect of chemotherapy is guaranteed. The medicine is simple in preparation process and high in stability, can realize efficient protection in a myocardial injury model, and has clinical application potential.

The invention belongs to the technical field of biological medicines, and provides application of CDCA7 and RUNX1 in screening of drugs for promoting macrophage infiltration in an esophageal squamous cell carcinoma immune microenvironment. The CDCA7 is low in expression, the RUNX1 is low in expression, and immune cell infiltration in an ESCC immune microenvironment is promoted. Experimental results show that the CDCA7 positively regulates the transcriptional level of the RUNX1, and the RUNX1 negatively regulates the transcriptional level of the CCL5, so that the CDCA7 indirectly negatively regulates the expression level of the CCL5. After the expression level of CDCA7 is increased, the expression level of CCL5 is reduced, and the chemotactic effect on macrophages, especially M0 and M1 type macrophages, is reduced, so that the infiltration of the M0 and M1 type macrophages is reduced. The CDCA7 can regulate and control the expression level of RUNX1 through transcription and indirectly influence the expression level of a chemotactic factor CCL5, so that the chemotactic effect of macrophages in a tumor microenvironment, especially M1 type macrophages, is influenced.

The current invention is related to the prevention and treatment of diseases including cancer, autoimmune disease, and infectious disease using chemokines and the receptors to which they agonize. It has been found that certain chemokines, including CXCL4, CXCL9, CXCL10, and CXCL12 as well as CCL5 have various effects on toll-like receptors in various cell types and these can be utilized for disease treatment and prevention.

The present invention relates to a method for diagnosing, predicting, predicting susceptibility to treatment, and / or classifying the onset, progression, and / or outcome of diseases or disorders of the female reproductive tract, particularly in the context of endometriosis, wherein the method determines biomarkers in Table 1, such as CCL5 and / or NEAT1. The present invention further relates to a pharmaceutical product for use in patients stratified according to the method of the present invention, and a composition comprising reagents for detecting biomarkers in Table 1 for the diagnosis of diseases or disorders of the female reproductive tract.

The invention relates to a tissue marker for proton radiation heart injury and application of the tissue marker. The tissue marker comprises one or more of a transcription marker and a protein marker. Wherein the transcription marker comprises one or more of PIK3R5, CCR7, IL7R, CD7, CD22, CR2, CCL5 and VAV1, and the transcription marker comprises one or more of PIK3R5, CCR7, IL7R, CD7, CD22, CR2, CCL5 and VAV1; and the protein marker comprises one or more of SIRT1 and HMGB1 (High Mobility Group Box 1). According to the invention, the differential marker is used as a potential biomarker of the radioactive heart loss, and a research method for researching the radioactive heart loss by using a mouse model is provided, so that a demonstrative research is provided for multi-omics analysis of the radioactive heart loss and explanation of an action mechanism of the radioactive heart loss.

The present invention relates to a composition comprising C-C motif chemokine ligand 5 (CCL5) for promoting the activation of bone marrow-derived stem cells. It is identified that, when CCL5, which is a niche-enhancing factor, is injected together with growth related oncogene beta (GROβ), which is known to promote the mobilization of hematopoietic stem cells from the bone marrow into peripheral blood, and AMD3100, which is a CXCR4 antagonist, the migration of hematopoietic stem cells from bone marrow to peripheral blood increases, and the engraftment rate also increases when the hematopoietic stem cells are injected into recipients undergoing bone marrow transplantation. Therefore, the CCL5 protein, GROβ, and the CXCR4 antagonist AMD3100 are provided as a composition for promoting the activation of bone marrow-derived stem cells, and thus bone marrow-derived stem cells activated thereby is provided as a novel therapeutic means for bone marrow diseases requiring bone marrow transplantation.

The invention belongs to the technical field of biological medicines, and particularly relates to application of a PAPSS1 gene in resisting melanoma and colorectal cancer. Based on CRISPR / Cas9 gene editing technology research, PAPSS1 gene deletion is found to significantly up-regulate expression of a chemotactic factor CCL5 by activating an NF-kappa B signal channel, and the effect can be blocked by an NF-kappa B inhibitor JSH-23. Meanwhile, the targeted PAPSS1 can effectively promote infiltration of T cells, especially CD8 + T cells, reverse the immunosuppression state of'immune desert type 'tumors and enhance the tumor immunotherapy effect. According to the application disclosed by the invention, the research for the first time discovers that the knockout of the PAPSS1 can effectively inhibit the growth of melanoma and colorectal malignant tumors, and reveals that the PAPSS1 has important significance on the treatment of melanoma and colorectal cancer by regulating and controlling an immune escape mechanism mediated by a chemotactic factor CCL5-CCR5 axis.

The invention discloses a liposome which is used for inhalation and has chemotactic factor tropism and lung focus microenvironment regulation and control capability. The nano drug delivery system comprises chemotactic factor binding peptide modified on the surface of a liposome and an FGF antagonist entrapped in the liposome, and the chemotactic factor binding peptide is at least one of receptor or binding domain sequences of chemotactic factors related to common lung diseases such as CXCL12, CCL2 and CCL5. The FGF antagonist is at least one of an FGFR tyrosine kinase inhibitor, an antibody targeting FGF or a receptor thereof, an FGF ligand trapping agent and siRNA targeting FGF or the receptor thereof. According to the invention, chemotactic factors enriched in a lung focus microenvironment are utilized to construct the liposome which is used for inhalation and has chemotactic factor tropism, so that regulation and control of the microenvironment are realized, and a new direction is provided for postoperative treatment of breast cancer.

Biomarker-based treatment, monitoring, and diagnostic methods for IL-17 dependent conditions, including hidradenitis suppurativa, are disclosed. The biomarkers may be selected from IL6, PLA2G2A, IL19, PI3, CST7, IL17A, IL17F, GH1, MZB1, IL1B, IFNG, TNC, CXCL9, SLAMF7, VEGFA, IL17C, SLAMF1, SDC1, OSM, LBP, REG3A, CD79B, COL4A1, CLEC4D, VWF, IL5RA, CSF3, TGFA, IL2RA, ITIH3, FCAR, CCL23, NRCAM, RETN, SERPINA11, CLEC4G, CSF1, HGF, CRELD2, EFEMP1, LTBR, NME3, CKAP4, CD276, SPON2, GGH, TIMP1, LY9, MCFD2, TCN2, QPCT, HYOU1, TNSFSF13B, CCL2, CCL3, CCL4, CCL5, CCL7, CCL20, CXCL1, CXCL8, PDFGA, CXCR2, CCR6, CXCL13, PCDH1, BOC, MEPE, ADAM23, THOP1, IL1RL2, RCOR1, EDAR, and combinations thereof. Kits for measuring the biomarkers, diagnosing and treating IL-17-dependent conditions, and identifying super-responders are also disclosed.