40 results about "Jurkat cells" patented technology

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 Lea structure, a Lea-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.

Humanized anti-CD11a antibodies and various uses therefor are disclosed. The humanized anti-CD11a antibody may bind specifically to human CD11a I-domain, have an IC50(nM) value of no more than about 1 nM for preventing adhesion of Jurkat cells to normal human epidermal keratinocytes expressing ICAM-1, and / or an IC50 (nM) value of no more than about 1 nM in the mixed lymphocyte response assay.

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 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 combined medicine for treating tumors. The combined medicine is prepared from unit preparations of an arsenic compound solution and a brazilin compound with different specifications, wherein the arsenic compound solution is prepared by the following steps: adding As2O3 powder into aseptic deionized water to obtain a suspension liquid, and dripping a NaOH solution into the suspension liquid until powder is completely dissolved. The brazilin compound consists of brazilin and brazilein. According to the combined medicine, an arsenic compound and a brazilin compound are combined, so that the curative effect of the arsenic compound can be improved, the dosage and corresponding toxic and side effects of the arsenic compound can be controlled, the combined medicine can be used more safely, and the therapeutic spectrum of the arsenic compound can be extended. The combined medicine has an especially excellent synergetic effect in the aspect of T-lymphoma cell line Jurkat cells.

The present invention relates to a Jurkat-KI-R5 and its construction method and application. The present invention knocks a powerful enhancer / promoter combination (CAG) into CD4+Jurkat T cells through CRISPR / Cas9 gene editing technology homologous recombination The promoter region of the CCR5 gene, and the genetically modified cell line was named Jurkat‑KI‑R5 cells. The precise recombination of the CAG promoter of Jurkat-KI-R5 cells according to the present invention to the specified position of the CCR5 promoter leads to stable and high expression of CCR5. In contrast to maternal Jurkat cells, Jurkat‑KI‑R5 cells are highly susceptible to HIV‑1 infection. Therefore, Jurkat‑KI‑R5 cells provide a much-needed cell platform for AIDS research.

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 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.