40 results about "Jurkat cells" patented technology

The present invention relates to assay methods used for detecting the presence of PIF, and to PIF peptides identified using this assay. In particular, the present invention relates to flow cytomery assays for detecting PIF. It is based, at least in part, on the observation that flow cytometry using fluorescently labeled antilymphocyte and anti-platelet antibodies demonstrated an increase in rosette formation in the presence of PIF. It is further based on the observation that flow cytometry demonstrated that monoclonal antibody binding to CD2 decreased in the presence of PIF. The present invention further relates to PIF peptides which, when added to Jurkat cell cultures, have been observed to either (I) decrease binding of anti-CD2 antibody to Jurkat cells; (ii) increase expression of CD2 in Jurkat cells; or (iii) decrease Jurkat cell viability. In additional embodiments, the present invention provides for ELISA assays which detect PIF by determining the effect of a test sample on the binding of anti-CD2 antibody to a CD2 substrate.

The present invention relates to a method for inducing and expanding natural killer cells derived from peripheral blood mononuclear cells, which comprises co-culturing, as feeder cells, irradiated Jurkat cells and irradiated Epstein-Barr virus transformed lymphocyte continuous line (EBV-LCL) cells in the presence of cytokines, along with peripheral blood mononuclear cells. According to the present invention, a large quantity of natural killer cells can be induced and proliferated from a small quantity of peripheral blood mononuclear cells even without the use of high-cost equipment or various kinds of expensive cytokines, thereby making it possible to significantly improve the efficiency and efficacy of the prevention and treatment of cancer using the natural killer cells.

The present invention provides novel antibodies specifically bind to an epitope on CD43 and CEA expressed on nonhematopoietic cancer cells, but do not specifically bind to a CD43 expressed by a leukocyte or by a Jurkat cell, and is capable of inducing apoptosis of the nonhematopoietic cancer cell after binding to the epitope on cell surface of the nonhematopoietic cancer cell in the absence of cytotoxin conjugation and immune effector function, wherein the epitope comprises a carbohydrate structure and the binding of the antibody to the epitope is inhibited by a carbohydrate comprising a Le^a structure, a Le^a-lactose structure, a LNDFH II structure, or a LNT structure. In addition, the present invention also provides use of the antibodies described herein for diagnostic and therapeutic purposes.

The invention relates to an application of a flavonoid compound, the flavonoid compound is 3, 3', 4', 5, 7-pentahydroxyflavone dihydrate, the ELISA and protein fluorescence quenching experiments provethat the compound can effectively inhibit interaction of PD-1/PD-L1 proteins, and has a strong affinity for PD-L1 protein. Cell clone number formation and ELISA detection of IL-2 secretion assay prove that the compound can effectively enhance the tumor killing activity of T lymphocyte Jurkat cells against MDA-MB-231 and NCI-H460 tumor cells as well as the expression level of IL-2, and then reverse T cellular immunosuppression. The research results of the application provide a drug for tumor immunotherapy targeting the PD-1/PD-L1 immunological test site.

The invention relates to Jurkat-KI-R5 and a construction method and application thereof. A powerful enhancer/starter combination (CAG) is knocked into a starter area of a CCR5 gene of a CD4+Jurkat T cell by a CRISPR/Cas9 gene editing technique in a homologous recombination way; the name of the gene-modified cell system is Jurkat-KI-R5 cell. The Jurkat-KI-R5 cell has the advantages that a CAG starter of the Jurkat-KI-R5 is precisely recombined into the specified location of a CCR5 starter, and the high expression of the CCT5 is stably caused; oppisite to a maternal line Jurkat cell, the Jurkat-KI-R5 cell is easily infected by HIV-1 (human immunodeficiency virus-1); a cell platform urgently demanded by the HIV disease study is provided by the Jurkat-KI-R5 cell.

The invention discloses a method for determining the biological activity of an LAG3 (Lymphocyte Activation Gene-3) protein binding molecule. The method comprises the step of detecting the activity ofan anti-human LAG3 antibody by a co-expression NFAT (Nuclear Factor of Activated T cells) reporting element and Jurkat cells of human LAG3 protein under the condition of coexistence of SED and Raji cells. The method provided by the invention can be used for rapidly and accurately detecting the activity of the molecule bound with human LAG3 protein.

The invention discloses fusion protein TAT-hGH of human auxin and cell-penetrating peptide TAT as well as a preparation method and application of the fusion protein TAT-hGH. A deoxyribonucleic acid (DNA) sequence of the fusion protein TAT-hGH, a carrier containing the DNA sequence and a host cell containing the carrier are encoded; and a method for preparing the fusion protein TAT-hGH by gene engineering is provided. The fusion protein TAT-hGH has the functions of promoting Jurkat cell proliferation activity and influencing a transcriptional level of insulin-like growth factor (IGF) I of downstream factors; and meanwhile, the fusion protein TAT-hGH has a function of penetrating through intestines. The fusion protein TAT-hGH can be orally taken, enters blood by penetrating through an intestinal cell membrane, and can reach different tissues by blood circulation, so that the utilization ratio of hGH is increased, and the medicinal effect is also improved. The preparation method can be applied to large-scale industrial production, and is high in expression amount, easy to operate and low in cost.

The invention discloses a method for transfecting Jurkat cells. The method comprises the following steps: adding 0.1mg/mL poly-D-lysine into a 24-pore cell culture plate, standing at the temperature of 4 DEG C overnight, sucking out liquid, uncapping and blowing in a super clean bench, and washing with a PBS (Phosphate Buffered Solution); inoculating Jurkat cells into the culture plate, culturing in an incubator, removing supernatant the next day, and washing with the PBS for 3 times to turn the Jurkat cell into a wall-attaching state; transfecting pLL3.7 plasmids according to conventional transfecting steps of wall-attaching cells; observing the expression amount of GFPs (Green Fluorescent Proteins) under a fluorescence microscope 24 hours after transfection in order to determine the transfecting efficiency. By adopting the method, the contact opportunity between a plasmid compound and cells can be increased after the Jurkat cells are subjected to wall-attaching treatment, and the transfecting efficiency is increased effectively (90 percent or more). The cell viability is not influenced by a wall-attaching treatment process, and exogenous plasmids can be transfected for the Jurkat cells safely.

The invention provides an anti-PD-L1/CD47 bispecific antibody and use thereof. Specifically, the invention provides a bispecific antibody which comprises (a) a PD-L1 single-domain antibody and (b) a CD47 single-domain antibody. The invention provides a coding sequence for coding the bispecific antibody, a corresponding expression vector, a host cell capable of expressing the bispecific antibody, and a production method of the bispecific antibody. The bispecific antibody can target PD-L1 and CD47 at the same time, can not only activate T cells, but also effectively promote phagocytosis of Jurkat cells by macrophages without causing human red blood cell agglutination, and has good application prospects.

The enzyme telomerase is present at about 85% of human cancers that makes it not only an excellent target for cancer treatment but also an excellent marker for cancer detection. Using a single stranded DNA probe specific for telomerase binding and reverse transcription tethered to an interdigital gold electrode array surface, the chromosome protection provided by the telomerase was replicated and followed by Electrochemical Impedance Spectroscopy as an unlabeled biosensor. Using a custom system, which is simple and affordable, the impedance measurements were taken while incubating at 37° C. and promoting the probe elongation. This resulted in up to 14-fold increase in the charge transfer resistance when testing a telomerase-positive nuclear extract from Jurkat cells compared to the heat-inactivated telomerase-negative nuclear extract. The electron transfer process at the Au electrodes was studied before and after the elongation, after 4 months in contact with the telomerase-positive nuclear extract, and after desorption of the non-specific bindings.

The invention discloses a method for measuring the activity of an anti-VEGF (Vascular Endothelial Growth Factor) antibody. An effector cell which transfects a VEGF receptor, IL-1R3, IL-1R6 and a reporter gene is taken as a detection material, anti-CD3 and anti-CD28 antibodies activate Jurkat cells, a VEGF ligand is added and is combined with a VEGFR (Vascular Endothelial Growth Factor Receptor) onthe effector cell, so that IL-1R3 and IL-1R6 in the cell mutually act to activate a downstream NFAT (Nuclear Factor of Activated T) signal path, and therefore, the reporter gene can be expressed. After the anti-VEGF antibody is added, the anti-VEGF antibody can be competitively combined with the VEGF ligand so as to block the combination of the VEGF ligand and the receptor VEGFR thereof so as toreduce a downstream reporter gene expression quantity. The method has the advantages of convenient operation step, high detection sensitivity and good accuracy, and experiment time is greatly shortened.

The invention relates to a method for extracting antitumor effective sites of selfheal, which comprises: using ethanol to soak spica of the selfheal in an extractor, and performing heating, reflux and extraction; concentrating an extracting solution into a dried extract, using chloroform and water or ethyl acetate and the water to extract the dried extract, respectively collecting an organic phase and an aqueous phase, and concentrating the organic phase and the aqueous phase to be dried; using the chloroform, methanol and the water to dissolve the organic phase, separating out superstratum after standing, and concentrating an upper solution to be dried; and adding a mobile phase to dissolve upper residue, performing reversed-phase column chromatography and elution, collecting 30 to 80 percent methanol eluent, concentrating eluent of various phases to be dried, and obtaining the antitumor effective sites. The in vitro experiments of the effective sites of the selfheal determined by the proposal of the method can obviously inhibit proliferation of Rajicells, Jurkat cells, K562 cells and 435S cells; and the in vivo experiments have tumor inhibitory efficacy on a He T lymphoma EL-4 cell mouse, and can prolong the life cycle of the He T lymphoma EL-4 cell mouse; and the antitumor effective sites of the selfheal have definite antitumor function and low toxicity.

The invention discloses a single cell array chip based on fluid dynamics, and belongs to the technical field of cell detection. The chip is formed by bonding a glass substrate and polydimethylsiloxane with a flow channel. The flow channel comprises a main channel, grooves and slits, the main channel is a snakelike flow channel, one groove and one slit form an auxiliary channel, the groove in each auxiliary channel is communicated with the corresponding slit, adjacent linear flow channel sections of the main channel are communicated through the auxiliary channels, and the auxiliary channels are arranged in parallel between the adjacent linear flow channel sections of the main channel to form a groove and slit array. For Jurkat cells, a single cell array with the cell occupancy and the single cell rate over 90% can be obtained, and the obtained living cell rate in the grooves is over 98%; the single cell array can be obtained fast to achieve the optimized single cell graphical effect; biochemistry characteristic analysis can be directly carried out on cells in the chip, observation is easy, and heterogeneity of the single cells can be detected.

The invention relates to a quinazoline compound. The structure of the compound is represented by a general formula shown in the specification. In the general formula, R is one of hydrogen, alkyl groups, alkenyl groups, alkynyl groups, aralkyl groups, formyl groups, halogens, nitro groups, amino groups, amido groups, acylamino groups, sulfonamide groups, hydroxy groups and alkoxy groups. The compound is a 4-{N-butyl-N-[(2'-1H-tetratriazol-5-yl)biphenyl)methyl]amine}quinazoline compound, and belongs to the field of medical immunology. The invention also relates to an application of the compound in the preparation of drugs for inhibiting Jurkat cell proliferation. The compound can well inhibit the Jurkat cell proliferation, and the drugs for inhibiting Jurkat cell proliferation prepared by using the compound can be used for autoimmune diseases and transplant rejection.

The present invention relates to a linear mimic peptide combined with cN-II. The linear mimic peptide has amino acid sequences as shown in SEQ ID NO:11-20. The mimic peptide can be combined with the cN-II, and has the antagonistic effect on the cN-II. The linear mimic peptide RP1 with the representative amino acid sequence as shown in the SEQ ID NO:11 can inhibit high expression of the cN-II in Jurkat cells, and co-culture can effectively improve the proliferation inhibition rate and the apoptosis rate of the cells under the action of araC and 6-MP, thereby reducing the drug resistance of thenucleoside analogs such as the araC and 6-MP in ALL disease treatment and the disease relapse.

The present invention relates to a mimetic peptide combined with cN-II. An amino acid sequence of the mimetic peptide is shown in SEQ ID NO:1-SEQ ID NO:10. The mimetic peptide can be combined with thecN-II and also has an antagonistic effect on the cN-II. The provided mimetic peptide cNMP represented by the SEQ ID No.1 can inhibit high expression of the cN-II in Jurkat cells and combined culturecan effectively improve proliferation inhibition rate and apoptosis rate of cells under actions of araC and 6-MP to reduce disease resistance and disease recurrence of nucleoside analogs such as the araC and 6-MP in treatment of acute lymphoblastic leukemia (ALL).

The invention discloses a making method of antihuman lymphocyte immunoglobulin, which is characterized by the following: adopting Jurkat cell system to replace human thymic lymphocyte as immunogen; reducing manufacturing cost without removing antibody step; fitting for large scale of manufacturing with high safe coefficient.

The invention relates to the technical field of biological medicines, and discloses a construction method of an acute T lymphocytic leukemia cytarabine drug-resistant cell strain. The construction method comprises the following steps: A, suspending leukemia cells Jurkat in a culture medium, and performing culturing in an incubator; B, continuously culturing the Jurkat cells in a complete culture medium containing 0.02 [mu]g/ml of Ara-C, and changing the liquid every 2-3 days; C, when the Jurkat cells can stably proliferate under action of the 0.02 [mu]g/ml of Ara-C, gradually increasing the concentration of the Ara-C, and repeatedly performing subculturing until the Jurkat cells stably survive under a condition that the concentration of Ara-C is 1 [mu]g/ml, so as to obtain the Jurkat/Ara-C-resistant cell strain, and detecting the drug resistance multiple; and D, continuously culturing the Jurkat/Ara-C cell strain for 1 month by using an Ara-C-free complete culture medium, and detectingthe drug resistance multiple again. The invention provides a new cell model for leukemia research.