46results about How to "Enhance tumor killing activity" patented technology

The invention discloses a method for preparing anti-tumor combined immune cells DC (dendritic cell)-CIKs (cytokine induced killers) and NKs (natural killers) simultaneously and the prepared combined immune cells. Ficoll density gradient centrifugation is used for efficient separation, a mononuclear cell is obtained, sufficient quantities of DCs, CIKs and NKs are obtained through cell culture bags and an immune cell induction culture system, and finally, the induced cells are cultured in a combined manner and applied to clinical treatment, so that a tumor killing effect is realized. The DCs, the CIKs and the NKs are subjected to induction culture respectively with adoption of TexMACS immune cell culture media produced by Miltenyi Biotec, autoserum, various cytokines and a combined culture technology, the cells are mixed for culture and application at certain point in time, application of fetal calf serum is avoided, the pollution rate of an exogenous pyrogen and an exogenous allergen is reduced, and the tumor killing activity of the finally mixed cells is enhanced simultaneously; with adoption of a cell culture bag technology, the cell contamination rate is reduced, and the method is suitable for clinical treatment and application.

The invention discloses a quasi-chimeric antigen receptor-modified CIK (cytokine induced killer) as well as a preparation method and the application thereof. The method for preparing a quasi-chimericantigen receptor-modified CIK cell preparation comprises the following steps: silencing 5'-UTR, 3'-UTR and / or an intracellular region of a CTLA4 mRNA in the CIK by using multiple serially-connected miRNAs, and expressing a CTLA4 extracellular region-CD28-41BB-CD3 fusion protein, so as to prepare the quasi-chimeric antigen receptor-modified CIK cell preparation. An experiment shows that the carriercan greatly reduce the expression of endogenesis CTLA4 in a CIK cell, and after the expressed CTLA4 extracellular region-CD28-41BB-CD3 fusion protein is combined with B7 on the surface of a cell T, the CIK cell is activated, thereby obviously improving the tumoricidal activity of the CIK cell.

The invention relates to application of a polypeptide XZZ-5 to induction and enhancement of tumor killing activity of CIK (Cytokine Induced Killer) cells. A research shows that the polypeptide XZZ-5 is used for inducing CIK or DC-CIK cells, and the multiplication and differentiation of the cells can be effectively enhanced, so that the tumor killing activity of the cells is improved; the application is hopefully developed to a brand new biological therapy manner.

The invention provides an astragalus extract FQR-8 and a preparation method and application thereof and further provides a method for using the FQR-8 to induce and culture CIK or DC-CIK cells. The preparation method comprises the steps of peripheral blood collection, tumor antigen obtaining, mononuclear cell separation, washing, induction and culture of the DC-CIK cells and the like. The astragalus extract FQR-8 prepared by means of the preparation method can effectively promote proliferation of the CIK cells, improve the tumor killing activity of the DC-CIK cells and prolong the survival time of a tumor-bearing mouse treated by using the DC-CIK cells.

The invention discloses a preparation method of human cytokine-induced killer cells, comprising the following steps: coating a cell culture flask with a coating buffer containing effective amount of fusion protein and human CD3 monoclonal antibody before culturing precursor cells of human CIK cells, and adding the human CD3 monoclonal antibody in the whole process of inducing and culturing the human CIK cells, wherein the fusion protein is human intercellular adhesion molecule-1 functional domain and human fibronectin functional domain fusion protein, and the concentration of the human CD3 monoclonal antibody in the cell culture solution is lower than the concentration of the human CD3 monoclonal antibody in the coating buffer. According to the invention, ex-vivo expansion efficiency of peripheral blood mononuclear cells and the proportion of CD3 / CD56 double positive cells in the CIK cells are significantly raised, the cytotoxicity activity of the CIK cells is enhanced, thus the effect of cellular immunity treatment is raised.

The invention relates to HPK1-targeted gRNA and an editing method aiming at an HPK1 gene. According to HPK1gRNA and the editing method of the HPK1 gene, the HPK1 gene of the T cell can be knocked out,the killing activity of the T cell can be improved, the Th1 cell factor level of a peripheral blood monouclear cell can be increased; and by knocking out the HPK1 gene of the T cell, the expression of PD-1 and TIM3 on the surface of the T cell can be decreased, and the failure of the T cell can be inhibited. Therefore, HPK1-targeted gRNA can be used for preparing tumor treatment drug and can be particularly applied to targeting therapy methods (CRA-T, CAR-NK, CAR-NKT and CAR-gammadelta) for chimeric antigen receptor cell tumors.

The invention relates to the technical field of biological cells, in particular to an immune cell and application thereof. A chimeric antigen receptor is expressed on the cytomembrane of the immune cell, and in addition, an immune checkpoint antibody protein fused with a cytokine receptor is also expressed on the cytomembrane. The expression CAR cell of the immune checkpoint antibody protein fused with the cytokine receptor is also expressed on the cytomembrane; through the immune checkpoint antibody protein which is fused with the cytokine receptor and is expressed on the immune cytomembrane, two negative feedback approaches PD-1 and CTLA-4 are blocked so as to weaken negative regulation and control of a tumor microenvironment for the immune cell, reduce exhaustion of the immune cell, enhance the tumor killing function of the immune cell and reduce inhibition of the immune cell by the tumor microenvironment; and in addition, through binding with the cytokine receptor, corresponding JAK and STAT signal channels are activated, and the cells are induced to secrete various active substances, including IFN-[gamma], perforin, granzyme and the like so as to inhibit growth of tumor cells, enhance an anti-tumor capacity, reduce the exhaustion and reduce the inhibition of the immune cell by the tumor microenvironment.

The invention relates to the field of virus and the field of tumor treatment. Concretely, the invention relates to ECHO 25 or a modified form thereof, or a genomic sequence or cDNA sequence comprisingthe ECHO 25 or the modified form of the ECHO 25, or nucleic acid molecules of a complementary sequences of the genomic sequence or cDNA sequence, applications in treating tumors for a subject such asa human being, and applications in preparing pharmaceutical compositions for treating the tumors for the subject such as a human being. The invention also relates to a method for treating the tumors.The method includes steps of applying the ECHO 25 or the modified form of the ECHO 25, or the genomic sequence or cDNA sequence comprising the ECHO 25 or the modified form of the ECHO 25 or the nucleic acid molecules of the complementary sequences of the genomic sequence or cDNA sequence to the subject who needs the treatment.

The invention relates to the technical field of biological medicine and oncology, in particular to a composite exosome loaded with membrane-bound tumor necrosis factor-related apoptosis-inducing ligand and small-molecule antitumor drug as well as a preparation method and application of the composite exosome. The membrane surface of the composite exosome carries TRAIL protein, and the small-molecule antitumor drug is entrapped in a membrane. A preparation process of the composite exosome is mature, efficient, good in reproducibility and low in cost. The composite exosome has the advantages of obvious in-vitro and in-vivo anti-tumor effects, low drug dosage, no toxic or side effect and good biological safety, and provides a new strategy for clinical treatment of tumors.

The invention provides a DC-CIK (dendritic cells-cytokine-induced killers) cell treatment composition derived from umbilical cord blood, wherein DC (dendritic cells) and CIK (cytokine-induced killers) cells are derived from single karyocyte of the same umbilical cord blood. The invention also provides a preparation method of the DC-CIK cell treatment composition. According to the cell treatment composition prepared by adopting the method, CIK cells are high purity and strong in multiplication capacity; the DC is high in purity and strong in antigen presentation capability, so that CIK cell multiplication can be effectively promoted, and the tumor killing activity of the CIK cell can be strengthened; compared with the simple CIK cells, the DC-CIK cells are higher in percentage of CD3<+> CD56<+> cells, and the tumor cell killing activity is remarkably higher.