78 results about "Cytotoxic T cell" patented technology

The invention belongs to the field of biological medicine, and relates to a method for preparing iTNK cells, prepared iTNK, a pharmaceutical composition of the iTNK and application of the iTNK. Specifically, the invention relates to a method for preparing iTNK cells, which comprises the following steps: (1) adding a proper amount of anti-CD3 / CD28 / CD2T cell Activator into a culture medium for culturing T cells; culturing for 1-4 days; preferably culturing for 2 days; (2) replacing the culture medium with a culture medium which does not contain anti-CD3 / CD28 / CD2T cell Activator, and continuously culturing for 20 to 30 days; preferably, the culture lasts for 26 days. The iTNK cell prepared by the method disclosed by the invention has dual attributes of cytotoxic T cells and NK cells and a tumor killing function, and has a good anti-tumor application prospect.

Activation of STimulator of INterferon Genes (STING) triggers cytokine production and facilitates tumor antigen cross-presentation. In an embodiment of the present invention, STING-dependent innate immune signaling pathway activators (STAVs) together with Replicants including mRNA adapted to express an antigen can be delivered to antigen presenting cells (APC's) using lipid nanoparticle formulations. In various embodiments of the present invention, the range of cancers amenable to STAV / Replicant therapy can be extended using a non-cell-based nanoparticle strategy that effectively delivers the STAV / Replicant into the Tumor Micro Environment (TME) to potently generate anti-tumor cytotoxic T cell activity together with humoral immune responses. The STAV / Replicant formulations can be introduced into solid tumors present in the subject. Alternatively, the STAV / Replicant can be introduced through direct inoculation, intramuscularly, or intravenously. The lipid nanoparticles stick to the tumor cells and are co-phagocytosed to activate STING in APC's.

The invention discloses an elephant source bacillus licheniformis and application thereof. The preservation number of the bacillus licheniformis strain L517 is GDMCC 67825, the bacillus licheniformis strain L517 is classified and named as bacillus licheniformis, and the preservation date is February 26, 2026. Research finds that the bacillus licheniformis has a remarkable treatment effect on acute colitis of mice; and the traditional Chinese medicine composition also has a remarkable treatment effect on mouse subcutaneous colon cancer. The anti-cancer mechanism is that the infiltration of GZMB < + > CD8 < + > cytotoxic T cells in a tumor microenvironment is remarkably promoted in vivo through a supernatant metabolite of a culture medium, and a tumor suppressor gene P53 can be directly up-regulated. It is found for the first time that the elephant intestinal tract source bacillus licheniformis with evolutionary disease-resistant advantages shows good anti-proctitis and colon cancer activity, and can become an effective medicine for treating proctitis and colon cancer in the future.

Activation of STimulator of INterferon Genes (STING) triggers cytokine production and facilitates tumor antigen cross-presentation. In an embodiment of the present invention, STING-dependent innate immune signaling pathway activators (STAVs) together with Replicants including mRNA adapted to express an antigen can be delivered to antigen presenting cells (APC's) using lipid nanoparticle formulations. In various embodiments of the present invention, the range of cancers amenable to STAV / Replicant therapy can be extended using a non-cell-based nanoparticle strategy that effectively delivers the STAV / Replicant into the Tumor Micro Environment (TME) to potently generate anti-tumor cytotoxic T cell activity together with humoral immune responses. The STAV / Replicant formulations can be introduced into solid tumors present in the subject. Alternatively, the STAV / Replicant can be introduced through direct inoculation, intramuscularly, or intravenously. The lipid nanoparticles stick to the tumor cells and are co-phagocytosed to activate STING in APCs.

To provide a novel chimeric antigen receptor-T cell (CAR-T cell) therapy, and to provide a medicament using the same.SOLUTION: Provided are: a method for producing T cell-derived induced Pluripotent Stem Cells (T-iPSCs) with two antigen receptors, comprising introducing, into cytotoxic T lymphocyte (CTL)-derived iPS cells (T-iPSCs) specific to a tumor antigen or viral antigen expressed on target cells, a chimeric antigen receptor (CAR) specific for an antigen different from the antigen; T-iPSCs with a T cell receptor (TCR) specific to a tumor antigen or viral antigen expressed on target cells and a CAR specific to an antigen different from the antigen; and furthermore, CTLs expressing a TCR specific to a tumor antigen or viral antigen expressed on target cells and a CAR specific to an antigen different from the antigen.SELECTED DRAWING: None

A nanoparticle and a preparation method therefor, the nanoparticle including an amphiphilic peptide, which forms a micelle structure through self-assembly, and a target peptide (preferably, a water-soluble antigen peptide), which electrically binds to the surface of the amphiphilic peptide. The target peptide electrically binds to the surface of the amphiphilic peptide micelle structure and becomes particulated, and thus can be effectively presented to an antigen-presenting cell, and the weight ratio of the amphiphilic peptide and the target peptide is controlled so that the size of nanoparticles is controlled and endocytosis thereof is carried out, and thus immunity by means of cytotoxic T cells can be induced. Nanoparticles exhibit use only an epitope of a more accurate region so as to be effective as a vaccine, and thus have minimal side effects. Therefore, excellent antigen-specific antibody and cell immunotherapy effects are exhibited, and thus can be used in various fields such as vaccine production.

CD38 is also expressed in a variety of hematological malignancies, including multiple myeloma. In the present invention, the inventors obtained a new antibody against CD38 that can be used to produce bispecific antibodies and CAR T cell populations. In particular, the inventors reported the development of Bi38-3, a new bispecific T cell engager that targets CD38 on MM cells and forms cytotoxic T cells through CD3ε. Bi38-3 lacks the Fc region of natural mAbs, which contributes to the resistance process, but triggers T cell proliferation, cytokine release, and lysis of CD38-positive MM cells in vitro. Similarly, Bi38-3 induces autologous T cells to eliminate tumor plasma cells isolated from MM patients at diagnosis and relapse. The cytotoxicity triggered by Bi38-3 is limited to cells expressing high levels of CD38 and maintains the integrity of T, B, and NK lymphocytes in vitro. Importantly, Bi38-3 rapidly reduced tumor cells in the MM1.S xenograft mouse model of human MM. In summary, the results show that the antibody of the present invention is an effective agent for specifically eliminating CD38-positive malignant cells without significantly affecting CD38-low-expressing cells, and is a promising new immunotherapy tool for treating malignant blood diseases, especially multiple myeloma.

The present invention relates to the field of medical materials technology, and in particular to an anti-tumor vaccine and its applications. The anti-tumor vaccine comprises anti-tumor nanoparticles comprising a nucleic acid encoding a plasma membrane vesicle-associated protein (PLVAP), a cationic lipid, and a non-cationic lipid. Research has shown that an anti-tumor vaccine based on an antigen molecule specifically expressed on tumor vascular endothelial cells (PLVAP) can effectively activate the immunosuppressive microenvironment of tumor patients, inducing the generation of a large number of cytotoxic T cells. These T cells are capable of targeting and killing tumor vascular endothelial cells expressing the PLVAP protein, effectively destroying tumor blood vessels. This vaccine holds significant value in the field of anti-tumor biomaterials.

A bispecific antibody, including: a first antibody or antigen-binding fragment thereof that specifically binds to a first antigen; a second antibody or antigen-binding fragment thereof that specifically binds to a second antigen; where the first antigen is TNFR2, and the second antigen is 4-1BB; or, the first antigen is 4-1BB, and the second antigen is TNFR2. The bispecific antibody is a T cell regulator of the tumor microenvironment, which can stimulate the proliferation of CD8+T cells, activate CD8+T cells, and release anti-tumor factors, such as IFNγ and IL2 by using a TNFR2 agonistic antibody, or can block TNF-TNFR2 and inhibit the proliferation of Treg by using a TNFR2 antagonistic antibody. The bispecific antibody can simultaneously target 4-1BB, activate the 4-1BB signaling pathway of T cells and NK cells, enhance the killing power of cytotoxic T cells and NK cells, and produce anti-tumor activity.

The invention discloses an application of an esterase response cationic polymer in preparation of an anti-tumor immunotherapy drug. The esterase response cationic polymer is an esterase response cationic polymer containing (p-phenolic ester group) benzyl amine or (p-phenolic ester group) benzyl ester. The compound can kill tumor cells, induce immunogen cell death (ICD), promote the tumor cells to release tumor-associated antigens, induce antigen-presenting cells to gather in tumors and present tumor antigens, activate killer T cells, inhibit tumor neovascularization, improve the tumor microenvironment, inhibit tumor cell apoptosis, inhibit tumor cell apoptosis, inhibit tumor cell apoptosis and inhibit tumor cell apoptosis after intratumor injection. Therefore, the organism obtains the anti-tumor immunity capability.

The present invention provides immunoresponsive cells, including T cells, cytotoxic T cells, regulatory T cells, and Natural Killer (NK) cells, expressing an antigen recognizing receptor and an inhibitory chimeric antigen receptor (iCAR). Methods of using the immunoresponsive cell include those for the treatment of neoplasia and other pathologies where an increase in an antigen-specific immune response is desired.

The present invention relates to a composition, for prevention or treatment of cancer diseases, comprising CD8+ T cells activated by CD4+ T cell-derived extracellular vesicles as an active ingredient. It was found that the secretion of extracellular vesicles from cytokine-activated CD4+ T cells increases and the extracellular vesicles enhance proliferation and activity of CD8+ T cells to induce the death of cancer cells, thereby augmenting an anticancer effect. Thus, the present invention provides the CD8+ T cells activated by CD4+ T cell-derived extracellular vesicles as a pharmaceutical agent or an immunotherapeutic agent for cancer diseases, and a method for activating CD8+ T cells by using CD4+ T cell-derived extracellular vesicles to prepare CD8+ T cells showing excellent anticancer activity as described above.

The present technology provides compositions and methods for modulating T Cell Receptor (TCR) specificity as well as methods for treating cancer in a subject in need thereof. The present disclosure provides engineered cytotoxic T cells comprising a TCR and / or nucleic acid encoding the TCR and a mutant CD8 alpha polypeptide and / or nucleic acid encoding the mutant CD8 alpha polypeptide.

A rapid detection method for cytotoxic T cells in peripheral blood. The method enables rapid identification of cytotoxic T cells in peripheral blood by detecting the expression of T-cell surface protein CX3CR1, or CX3CR1 and GPR56. The detection method is rapid in operation, does not involve cell fixation and permeabilization, and does not affect cell activity.

Provided is a method for evaluating the efficacy of an anticancer drug using a mixture of peripheral blood mononuclear cells and cancer organoids; a method for screening the anticancer drug; a system for evaluating the efficacy of the anticancer drug; or a system for screening the anticancer drug. Specifically, the present invention relates to: a method for evaluating the efficacy of an anticancer drug using a mixture of cytotoxic T cells differentiated from PBMCs and cancer organoids; a method for screening the anticancer drug; a system for evaluating the efficacy of the anticancer drug; or a system for screening the anticancer drug. The method for evaluating the efficacy of an anticancer drug, the screening method, the efficacy evaluation system, or the screening system according to the present invention can very closely reproduce a tumor microenvironment, which is the form in which cancer cells exist in a living body.

Disclosed is a method for producing activated cytotoxic T cells derived from iPS cells, the method comprising the following steps (1): (1) activating non-activated cytotoxic T cells derived from iPS cells in a container having excellent gas exchange performance; a method for proliferating activated cytotoxic T cells derived from iPS cells, the method comprising the following steps (1A): (1A) activating non-activated cytotoxic T cells derived from iPS cells in a container having excellent gas exchange performance; a cell population comprising the activated cytotoxic T cells obtained by the method; and a drug comprising the cell population comprising the activated cytotoxic T cells.

The purpose of the present invention is to provide a cancer vaccine composition effective for treating or preventing cancer. The present invention provides a genetically modified cancer cell comprising: a nucleic acid encoding a cytotoxic T cell-inducing antigen and a nucleic acid encoding IL-2. This genetically modified cancer cell can be used as an active ingredient of a cancer vaccine composition. The cytotoxic T cell-inducing antigen in this genetically modified cancer cell is preferably a pathogen-derived antigen or a virus-derived antigen.

A method for generating antigen-specific CD4+ cytotoxic T cells comprising providing a plurality of CD4+ T cells; stimulating the CD4+ T cells with at least one tumor associated-antigen (TAA) peptide and / or at least one viral peptide; and expanding the CD4+ T cells in the presence of at least one pro-inflammatory cytokine. Also provided are enriched populations and compositions comprising the generated antigen-specific CD4+ cytotoxic T cells, and methods of treating, ameliorating, or preventing cancers and disease by administering the cells to subjects.

The invention relates to application of a dry memory T cell in preparation of a medicine for treating colorectal cancer pulmonary metastasis, and belongs to the technical field of biological medicine. The invention firstly proves that the capability of differentiating the Tscm cells into effector killer T cells can be effectively improved by knocking out the Erbin genes in the Tscm cells in a mouse body, lung metastasis of colorectal cancer is inhibited, and the treatment effect of CAR-T cells can be enhanced by the Tscm cells with the Erbin genes knocked out. In addition, xanthine is detected for many times in a mouse colorectal cancer lung metastasis focus after the Erbin gene in the Tscm cell is knocked out, hypoxanthine can promote generation of more Tscm cells in the tumor metastasis focus, and the Tscm cells are differentiated to generate killer T cells, so that colorectal cancer lung metastasis is inhibited. The metabolic pathway of hypoxanthine is further studied, it is found that allopurinol can inhibit conversion of hypoxanthine into xanthine and uric acid, and it is found that allopurinol can also inhibit colorectal cancer lung metastasis by injecting allopurinol into a colorectal cancer lung metastasis mouse model.

The present invention provides the induction of novel Th1 response, the induction of cytotoxic T cells and anti-cancer / anti-allergic activity techniques. Provided is a combination of a CpG oligonucleotide and an STING agonist. Also provided is a composition which contains an STING agonist, can be used as a type-I adjuvant, and is characterized in that the STING agonist is administered together with a CpG oligonucleotide. Further provided is an anti-cancer agent comprising a CpG oligonucleotide and is characterized in that the CpG oligonucleotide is administered together with an STING agonist. Still further provided is a composition which contains a CpG oligonucleotide and can be used for reducing or eliminating the IgE-inducing activity of an STING agonist.

The application discloses application of a small-molecule compound LZ-A4 in preparation of a preparation or a medicine for treating malignant tumors. 19 H 11 Cl2N3O3S, which can promote LGMN degradation in malignant tumor cells, inhibit tumor cell proliferation, and inhibit macrophage polarization to M2 type. The application proves through research on a colorectal cancer mouse transplanted tumor model that LZ-A4 alone can effectively inhibit the progression of colorectal cancer, and after being combined with a colorectal cancer first-line chemotherapy medicine oxaliplatin, the tumor volume can be further reduced. Meanwhile, LZ-A4 can inhibit M2 type polarization of macrophages in a tumor microenvironment in vivo, promote infiltration of cytotoxic T cells, reshape the tumor microenvironment, and activate anti-tumor immunity. In addition, A4 performs well in terms of toxic side effects, and after being combined with the chemotherapy medicine, the mouse weight is not further reduced.

In the present invention, the applicant provides a novel method of prophylactically or therapeutically treating acquired immunodeficiency syndrome (AIDS) in a subject in need thereof, where the subject is a human immunodeficiency virus (HIV) serum positive patient. Applicant also provides a novel method of preventing acquired immunodeficiency syndrome (AIDS) in a subject in need thereof, wherein the subject is a human immunodeficiency virus (HIV) serum negative patient. Applicant also provides a novel method of prophylactic or therapeutic treatment of acquired immunodeficiency syndrome (AIDS) in a subject in need thereof, wherein the subject is an elite controller patient that is serum positive for human immunodeficiency virus (HIV).

The invention belongs to the field of polymer chemistry and biomedical engineering, and discloses a construction method and application of a biomimetic membrane coated drug-loaded nano system. According to the system disclosed by the invention, small-molecule traditional Chinese medicine (sinomenine) is loaded in mesopores, and homologous cell membranes wrap drug-loaded nanoparticles to obtain a final nano-drug system which can effectively and passively target nasopharyngeal carcinoma cells. The sinomenine can cooperate with photothermal therapy to jointly induce mitochondrial injury, promote cell apoptosis and cause ICD immunoreaction, the sinomenine inhibits PD-L1 expression to relieve immunosuppression of T cells, meanwhile, infiltration of cytotoxic T cells in tumor sites is increased, distant metastasis of nasopharyngeal carcinoma can be inhibited by inhibiting MMPs and PD-L1, and the nasopharyngeal carcinoma can be inhibited by inhibiting MMPs and PD-L1. Therefore, the effects of enhancing nasopharynx cancer immunotherapy and inhibiting metastasis are achieved.

This invention relates to the fields of microbiology and biomedicine, and particularly to a strain of *Lactobacillus brittlemi* SYSU-32 and its application in tumor treatment. This invention cultured and isolated a strain of *Lactobacillus brittlemi* (SYSU-32). Limosilactobacillus pontis SYSU-32 was deposited on September 15, 2025, at the China General Microbiological Culture Collection Center (CGMCC), with accession number CGMCC No. 35919. This strain can increase CD8+ in the tumor microenvironment. + Infiltration of T cells and cytotoxic T cells inhibits the progression of colorectal cancer. Furthermore, the combination of *Lactobacillus bridgedii* SYSU-32 with the chemotherapy drug oxaliplatin enhances the pro-apoptotic effect of oxaliplatin, further inhibiting tumor progression and metastasis.

The present invention provides an adjuvant comprising a B-type CpG oligodeoxynucleotide (CpG ODN), a modification thereof, or a complex thereof, to be administered together with an mRNA vaccine in which mRNA is encapsulated in particles. The adjuvant contains the B-type CpG ODN that is present independently of the particles that encapsulate mRNA. This adjuvant can enhance antigen-specific cytotoxic T cell (CTL) induction by mRNA vaccines.

The invention relates to the technical field of biological medicines, in particular to a dendritic cell vaccine for multiple myeloma as well as a preparation method and application of the dendritic cell vaccine, and the dendritic cell vaccine is obtained by co-culturing dendritic cell vaccines MOLP-8, RPMI-8226, NCI-H929, U266B1 and MM1. S whole cell line lysates and dendritic cells. According to the present invention, the whole cell line lysates of MOLP-8, RPMI-8226, NCI-H929, U266B1 and MM1. S are adopted as the antigen of the DC vaccine, and the mixed lysates contain rich tumor antigens, can activate the immune system, and can generate the cytotoxic T cells aiming at the multiple myeloma antigens so as to specifically kill the tumor cells. The DC vaccine prepared by the invention not only stimulates T cells to generate more IFN-gamma, but also induces to generate stronger tumor killing T cells, and provides a new thought for research and development of multiple myeloma DC vaccines.

The present technology provides compositions and methods for modulating T Cell Receptor (TCR) specificity as well as methods for treating cancer in a subject in need thereof. The present disclosure provides engineered cytotoxic T cells comprising a TCR and / or nucleic acid encoding the TCR and a mutant CD8 alpha polypeptide and / or nucleic acid encoding the mutant CD8 alpha polypeptide.

The invention belongs to the technical field of cell culture, and discloses a multiplication culture method of tumor infiltrating lymphocytes, which comprises the following steps: S1, collecting and combining separated TILs cells, repeatedly cleaning and centrifuging by using a PBS buffer solution, and collecting cell precipitates; s2, suspending the cleaned cell precipitate in a T cell amplification culture medium, and performing double dispersion and transfer to new holes; and S3, continuously culturing in a 5% CO2 incubator at 37 DEG C. The T cell amplification culture medium comprises a T cell basal culture medium, human AB serum, an IL-2 solution, an IL-12 solution, an IL-15 solution, an IL-21 solution and a CD3 / CD28 costimulatory factor solution. According to the multiplication culture method provided by the invention, the TILs can be quickly amplified to a ten-million-level quantity in a short time, meanwhile, the specific amplification of regulatory T cells induced by IL-2 can be prevented, the differentiation of immature immune cells in the TILs towards CD8 + cytotoxic T cells is promoted, the quantity of the cytotoxic T lymphocytes is increased, and the differentiation rate of the T lymphocytes is increased. Therefore, the success of a TILs-based cell reinfusion therapy is increased.

The invention belongs to the technical field of biological medicine, and particularly relates to a copper death nano preparation based on logic gating as well as a preparation method and application of the copper death nano preparation. The invention provides a probe group for targeting tumor and a related nano preparation. The preparation is based on tumor biomarkers GSH and miRNA and DNA repair enzyme APE1, and has a nucleic acid cascade line of targeted silence tumor GLUT1. According to the invention, the synthesis route of [Cu (tz)] is improved, and nucleic acid line elements and copper ions are selectively released at the tumor site; through stimulation of an endogenous marker, a gene silencing function and a fluorescence signal of an activation line, inhibition of glycolysis of tumor cells and enhancement of oxidative phosphorylation are caused, copper ions can be cooperated to sensitize tumor cell copper death, and meanwhile, the killing ability of cytotoxic T cells to tumor cells is enhanced; remodeling an immunosuppressive tumor microenvironment and preventing immune escape; and finally, accurate tumor imaging recognition and efficient combined treatment based on copper death are realized.