34 results about "CCL5" patented technology

The present invention provides, inter alia, kits for selecting a chemotherapy regimen for a subject. The kits comprise one or more components for detecting the expression of at least one gene from the group of SLC12A7, GZMB, TAF6L, NFIB, METRN, ROPN1B, TTK, CCND1, PTTG1, H2AFZ, WDR45L, DEK, MCM2, USP1, CDT1, TMEM97, RER1, MCM6, LZTFL1, C11orf17, CCL5, XCL1, XCL2, MELK, CTSL2, TPX2, AURKA, CDKN2C, BRP44, PNP, SMC4, NR4A2, C3orf37, MTPAP, CDC25B, ABCF1, MTAP, SNAPC3, RANBP9, COIL, FAM86B1, ITGA6, S100P, RANBP1, PRSS16, SMARCA2, STK24, TSPYL5, SRI, LRP12, CENPF, TUBD1, KIAA1324, DBF4, CCNA2, DLGAP5, FHL1, SIRT3, GTSE1, PCNA, CCNE2, CHD3, CAP1, GPM6B, GUSBP3, GNAI3, LMO4, PSRC1, USP1, STK38, BAT2L1, PMP22, NME5, CENPA, BANK1, and derivatives thereof. Methods for selecting a chemotherapy regimen for a subject are also provided.

An antikine antibody binds to two, three, four, five or more CC chemokines, such as RANTES / CCL5, MIP-1α / CCL3, MIP-1β / CCL4, or MCP-1 / CCL2. Methods for affinity maturation and humanization of antikine antibodies as well as the production of hybridoma cell lines producing antikine antibodies by sequential immunization are also disclosed.

The present invention provides diagnostic methods, therapeutic methods, and compositions for the treatment of cancer. The compositions and methods described herein can be used, for example, to determine the propensity of a patient to benefit from treatment with a PD-L1 axis binding antagonist and to treat such patients accordingly. Using the compositions and methods of the disclosure, a patient, such as a human cancer patient, may be determined to be likely to benefit from treatment with a PD-L1 axis binding antagonist if the patient exhibits an elevated pre-treatment expression level of one or more of CST7, NKG7, GZMH, MT-ND4, HLA-H, CCL5, CD8A, CMC1, CD8B, HCST, MT-CYB, MT-ND4L, KLRG1, MT-CO2, MT-ATP6, PLEK, CTSW, HLA-C, LYAR, LITAF, GZMB, KLRD1, FGFBP2, KLRC4-KLRK1, KLRK1, B2M, GZMA, ID2, CX3CR1, PRSS23, GNLY, PRF1, and PATL2. Exemplary PD-L1 axis binding antagonists that may be used in conjunction with the compositions and methods of the disclosure are PD-L1 binding antagonists, such as anti-PD-L1 antibodies and antigen-binding fragments thereof, including atezolizumab, as well as PD-1 binding antagonists, such as anti-PD-1 antibodies and antigen-binding fragments thereof.

The present invention provides a method for predicting the treatment response to anti-cancer immunotherapy of a mammalian cancer patient, the method comprising: a) measuring the gene expression of atleast 2 the following cancer promoting genes: PTGS2, VEGFA, CCL2, IL8, CXCL2, CXCL1, CSF3, IL6, IL1B and IL1A in a sample obtained from the tumour of the patient; b)measuring the gene expression of atleast 2 of the following cancer inhibitory genes: CXCL11, CXCL10, CXCL9, CCL5, TBX21, EOMES, CD8B, CD8A, PRF1, GZMB, GZMA, STAT1, IFNG, IL12B and IL12A in a sample obtained fromthetumour of the patient; c) computing a ratio of the gene expression of said at least 2 cancer promoting genes and the gene expression of said at least 2 cancer inhibitory genes; and d) making a prediction of the treatment response and / or prognosis of the patient based on the gene expression ratio computed in step c). Also provided are related methods for stratifying patients and for treating patients, including withimmune checkpoint blockade therapy.

The invention relates to a marker for cancer cell drug resistance, a preparation composition for reversing cancer cell drug resistance and application of the preparation composition. The marker comprises a CCL5 chemotactic factor of cancer-related fibroblasts and a gene coded by the CCL5 chemotactic factor, and the expression level of the CCL5 chemotactic factor is positively correlated with the drug resistance of cancer cells. The preparation combination comprises a PARP inhibitor for inhibiting cancer cell replication and a reversal agent for regulating the cancer cell drug resistance caused by PARP. The reversal agent includes at least one of a regulator that down-regulates the expression of cancer-associated fibroblasts CCL5, a neutralizing antibody of CCL5, and an NF-[kappa] B signal inhibitor. The CCL5 expression related regulator, the CCL5 neutralizing antibody and / or the targeted NF-kappa B inhibitor are / is adopted to reverse the CAFs activation effect induced by the PARP inhibitor, the cancer cell drug resistance caused by the PARP inhibitor is inhibited, and the cancer cell killing effect of the PARP inhibitor is improved.

The present invention provides, inter alia, kits for selecting a chemotherapy regimen for a subject. The kits comprise one or more components for detecting the expression of at least one gene from the group of SLC12A7, GZMB, TAF6L, NFIB, METRN, ROPN1B, TTK, CCND1, PTTG1, H2AFZ, WDR45L, DEK, MCM2, USP1, CDT1, TMEM97, RER1, MCM6, LZTFL1, C11orf17, CCL5, XCL1, XCL2, MELK, CTSL2, TPX2, AURKA, CDKN2C, BRP44, PNP, SMC4, NR4A2, C3orf37, MTPAP, CDC25B, ABCF1, MTAP, SNAPC3, RANBP9, COIL, FAM86B1, ITGA6, S100P, RANBP1, PRSS16, SMARCA2, STK24, TSPYL5, SRI, LRP12, CENPF, TUBD1, KIAA1324, DBF4, CCNA2, DLGAP5, FHL1, SIRT3, GTSE1, PCNA, CCNE2, CHD3, CAP1, GPM6B, GUSBP3, GNAI3, LMO4, PSRC1, USP1, STK38, BAT2L1, PMP22, NME5, CENPA, BANK1, and derivatives thereof. Methods for selecting a chemotherapy regimen for a subject are also provided.

The invention discloses a recombinant vaccinia virus rVV-CCL5-SSTR2-Luc+, containing genes CCL5 and SSTR2, constructed by virtue of a homologous recombination method. By utilizing the characteristic that shuttle plasmids containing human target genes CCL5 and SSTR2 and Luciferase reporter genes have same TK side wings with a vaccinia virus WR strain, homologous recombination is carried out in a vaccinia virus susceptible cell BS-C-1 to integrate the target genes to a vaccinia virus genome, so as to construct the recombinant vaccinia virus rVV-CCL5-SSTR2-Luc+. The recombinant vaccinia virus rVV-CCL5-SSTR2-Luc+ is capable of efficiently expressing exogenous genes, meanwhile, CCL5 is matched with highly expressed CCR5 on the surface of a cell CIK, and SSTR2 has the unique advantage on directional induction of octreotide targeted tumor cells, so that the recombinant vaccinia virus is beneficial to clinical expansion and application and is used for treating various tumors.

The invention relates to the field of biotechnology, and the invention discloses a use of CCL5. The present invention utilizes the chemotactic binding ability of CCL5 and immune cell surface receptors such as DC cells to transport different antigenic proteins to the surface of DC cells, improves the efficiency of phagocytosis, processing and presentation of various antigenic proteins by DC cells, and improves the efficiency of DC cells. The effect of preventing and treating related diseases. The present invention also adds T2 sequence to the antigen so as to enhance the immune effect.

The invention discloses a method for enhancing mesenchymal stem cell chemotactic capacity and chemotactic factor CCL5 expression, and relates to mesenchymal stem cells. The method comprises the steps of separation of the mesenchymal stem cells and passage of primary culture umbilical cord mesenchymal stem cells; identification of the umbilical cord mesenchymal stem cells; stimulation of TNF-alpha and IFN-gamma to hUC-MSCs; detection of CCL5 expression through Real-Time PCR; detection of CCL5 expression through ELISA. CCL5 expression through MSCs is improved by 924 times, a large amount of natural CCL5 can be obtained, no lipofection transfection is needed, and rapidness and convenience are achieved. Due to simulation of TNF-alpha and IFN-gamma, the transfer ability of the mesenchymal stem cells is improved, it is promoted that the mesenchymal stem cells can more rapidly collect tissue injuries and inflammation portions in vivo, and the functions of tissue repairing and immune modulating are brought into play.

CC-Chemokine mutants having reduced Glycosaminoglycans (GAG)-binding properties are effective against liver fibrotic inflammatory and / or autoimmune diseases. Particularly preferred are the mutants of CCL5 / RANTES having reduced GAG-binding properties.

The invention belongs to the field of biological medicine, and particularly relates to the application of a chemotactic factor serving as a rosacea related molecular marker in diagnosis and treatment of the rosacea related molecular marker. The expression of TLR2 and chemotactic factors CCL5, CXCL9, CXCL10 and CXCL11 in rosacea animals induced by LL-37 is increased, and the AhR agonist benvimod can relieve erythema and inflammatory cell infiltration and reduce the expression of the TLR2 and the chemotactic factors. The expression of TLR2 and chemotactic factors CCL5, CXCL9, CXCL10 and CXCL11 in a rosacea cell model induced by LL-37 is increased, and the expression of TLR2 and the chemotactic factors can be reduced by an AhR agonist, namely, benvimod; the up-regulation of the TLR2 can cause the increase of the expression of the chemotactic factor in the cell model, and the AhR agonist benvimod can reduce the expression of the chemotactic factor by down-regulating the expression of the TLR2. The chemotactic factors CCL5, CXCL9, CXCL10 and CXCL11 are expected to become new diagnosis indexes or treatment targets of rosacea diseases.

The present invention relates to an engineered immune cell that expresses (i) a chimeric receptor, and (ii) an exogenous CCL3, CCL4 and / or CCL5. The invention also provides application of the engineered immune cell in treatment of cancer, infection or autoimmune diseases. Compared with traditional engineered immune cells, the engineered immune cells provided by the invention have significantly improved tumor killing activity.