31 results about "Cytotoxic T cell" patented technology

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.

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.

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.

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.

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.

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 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.

An antigen-loaded nanogel is formed by loading or encapsulating one or more long peptide antigens or one or more protein antigens in a hydrophobized polysaccharide. The long peptide antigen(s) or protein antigen(s) contains (or each contain) one or more CD8+ cytotoxic T cell recognition epitopes and / or one or more CD4+ helper T cell recognition epitopes, which is / are derived from the antigen. The antigen-loaded nanogel is administered at least one day prior to administration of antigen-specific T cells to improve the efficacy of a T cell infusion therapy against an immune checkpoint inhibitor-resistant tumor. The hydrophobized polysaccharide may be pullulan having cholesteryl groups bound thereto. An immune-enhancing agent also may be administered in or with the antigen-loaded nanogel.

The present invention provides CDCA1-derived epitope peptides having the ability to induce cytotoxic T cells. The present invention also provides polynucleotides encoding the peptides, antigen-presenting cells presenting the peptides, and cytotoxic T cells targeting the peptides, as well as methods of inducing antigen-presenting cells or CTLs. The present invention also provides compositions and pharmaceutical compositions containing them as active ingredients. Furthermore, the present invention provides methods of using the peptides, polynucleotides, antigen-presenting cells, cytotoxic T cells, or pharmaceutical compositions of the present invention to treat and / or prevent cancer, and / or prevent postoperative recurrence thereof. Methods of inducing an immune response against cancer are also provided.

The present invention relates to a highly active transposase protein for a transposon system and its uses. By improving the activity of the transposase, genes can be delivered effectively, which can be useful for developing genome-modified cell lines that express various genes. In addition, when T cells are transformed using the highly active transposase of the present invention, cytotoxic T cells (CD8) that have anti-cancer effects can be generated. + The proportion of T cells increases, and T cells persist in the body. CM (Central memory T cell), T SCM Since the proportion of memory-type T cells (stem cell-like memory T cells) increased, it is expected that TCR-T cells and CAR-T cells with good in vivo persistence can be produced using the transposon system of the present invention.

The present invention provides CDCA1-derived epitope peptides having the ability to induce cytotoxic T cells. The present invention also provides polynucleotides encoding the peptides, antigen-presenting cells presenting the peptides, and cytotoxic T cells targeting the peptides, as well as methods of inducing antigen-presenting cells or CTLs. The present invention also provides compositions and pharmaceutical compositions containing them as active ingredients. Furthermore, the present invention provides methods of using the peptides, polynucleotides, antigen-presenting cells, cytotoxic T cells, or pharmaceutical compositions of the present invention to treat and / or prevent cancer, and / or prevent postoperative recurrence thereof. Methods of inducing an immune response against cancer are also provided.

This invention discloses a sensitizer for PD-1 antibody drugs and its application, as well as an antitumor drug composition and its application. The sensitizer comprises dihydroartemisinin and niraparib, and the antitumor drug composition comprises dihydroartemisinin, niraparib, and a PD-1 antibody. This invention is the first to experimentally discover that dihydroartemisinin possesses a dual mechanism of action: "non-HRD-dependent PD-L1 upregulation" and "tumor-selective ferroptosis induction." This mechanism complements and synergizes with niraparib's "HRD-dependent PD-L1 upregulation + synthetic lethality" mechanism and the PD-1 antibody's "immune activation" mechanism. The antitumor drug composition formed by combining these three components can effectively reshape the tumor immune microenvironment, exerting a potent antitumor effect by upregulating PD-L1 expression in tumor cells, increasing the number of cytotoxic T cells, and inhibiting the proportion of regulatory T cells.

The present disclosure provides CyCAT half-body molecules and complementary pairs of such half-body molecules capable of associating with each other on the surface of a cell expressing two target antigens of interest. The tri-specific heterodimeric antibody molecules thus formed on the cells and on the target are able to engage and stimulate cytotoxic T cells to disrupt tumor cells. The disclosure further provides half body molecules having sterically hindered moieties attached thereto that reduce heterodimer formation of such half bodies in the presence of only one target antigen of interest or in the absence of two target antigens of interest.

Provided herein are immunogenic polypeptides, compositions, and methods related to the development of CMV-specific prophylactic and / or therapeutic immunotherapies based on cytotoxic T cell (CTL)-recognized T cell epitopes (e.g., CMV epitopes), and can be used to prevent and / or treat CMV infection, reactivation, and / or disease (e.g., CMV-associated end-organ disease), especially in solid organ transplant recipients.

This application relates to the field of diagnostic reagents, specifically to a scar diagnostic reagent and its application. This application is the first to discover CD3+ in the peripheral blood of keloid patients. + CD8 + The study revealed a significant decrease in cytotoxic T cells, highlighting for the first time the crucial role of the immune microenvironment in the pathogenesis of keloids. Furthermore, it was the first time that sHLA-E expression was significantly different in normal individuals compared to patients with hypertrophic scars and keloids. Using sHLA-E as a diagnostic marker can differentiate between hypertrophic scars and keloids, which are traditionally considered pathological scars, and can also be used to assess the effectiveness of keloid treatment.

The present disclosure provides in vitro modified cytotoxic T cells (CTLs) that comprise: a) a T-cell receptor (TCR) specific for a preselected antigen in a human; and b) a nucleic acid(s) encoding a chimeric antigen receptor (CAR) specific for a cancer-associated antigen. The present disclosure provides methods of producing the modified CTLs. The present disclosure provides methods of treating cancer, comprising administering the modified CTLs to an individual in need thereof.

The present invention relates to peptides, nucleic acids and cells for use in immunotherapeutic methods. In particular, the present invention relates to the immunotherapy of cancer. The present invention furthermore relates to tumor-associated cytotoxic T cell (CTL) peptide epitopes, alone or in combination with other tumor-associated peptides that serve as active pharmaceutical ingredients of vaccine compositions that stimulate anti-tumor immune responses. The present invention relates to 30 peptide sequences and their variants derived from HLA class I and class II molecules of human tumor cells that can be used in vaccine compositions for eliciting anti-tumor immune responses.

The present disclosure provides modified cytotoxic T cells (mCTLs), where the mCTLs comprise: a) one or more nucleic acids comprising nucleotide sequences encoding a T-cell receptor (TCR) specific for MHC class I polypeptides that present a human papilloma virus (HPV) E7 peptide comprising the amino acid sequence YMLDLQPETT (SEQ ID NO:1) or YMLDLQPET (SEQ ID NO:2); and b) one or more nucleic acids comprising nucleotide sequences encoding a chimeric antigen receptor (CAR), where the CAR comprises an antigen-binding domain specific for a cancer-associated antigen. The present disclosure provides methods of producing the mCTLs. The present disclosure provides methods of treating cancer, comprising administering the mCTLs to an individual in need thereof.

Providing C-type natriuretic peptides and methods for treating cancer. [Solution] The present disclosure relates to a method for treating a subject having an abnormal vascular system, comprising administering to the subject a therapeutically effective bolus dose of a composition comprising long-acting C-type natriuretic peptide (CNP), a CNP derivative, a long-acting CNP derivative, a long-acting CNP receptor (NPRB) agonist, or any combination thereof. The present disclosure further relates to treating a subject for which it is necessary to increase the activity of cytotoxic T cells and / or NK cells, comprising administering to the subject a therapeutically effective bolus dose of a composition comprising long-acting C-type natriuretic peptide (CNP), a CNP derivative, a long-acting CNP derivative, a long-acting CNP receptor (NPRB) agonist, or any combination thereof.

The invention belongs to the technical field of cancer treatment, and discloses application of co-targeting EZH2 / DNMT to synergistically reversing castration-resistant prostate cancer resistance. We prove that dual targeting of DNMT and EZH2 breaks epigenetic transformation, so that tumors are re-sensitive to androgen deprivation therapy. The strategy not only eliminates CRPC in a preclinical model, but also reverses immunosuppression, so that cytotoxic T cell infiltration is increased by 11.4 times. We data extend the use of EZH2 inhibitors beyond PRC2 dependent cancers, localizing the interaction of DNA methyltransferase with EZH2 as a targeting weakness in extracellular matrix rich solid tumors. The combination therapy provides a mandatory solution to overcome stromal disorders, which provides a revolutionary strategy for biomechanical factor driven malignancies.

The invention discloses an ultrasonic activated MnS-MOF-coated HM nano material, a preparation method and application thereof. The MnS-MOF-coated HM nano material takes manganese sulfide MnS as a manganese source to synthesize a metal organic framework MnS-MOF as a core and coats a hybrid membrane HM of a tumor cell membrane and a bacterial membrane. Under the activation of ultrasonic waves, the MnS-MOF-HM nano material can exert enzyme-like catalytic activity in a tumor slightly acidic environment, efficiently generate active oxygen ROS and release hydrogen sulfide H2S, and synergistically induce tumor cells to generate immunogenic death. Meanwhile, the immunologic adjuvant effect of the bacterial membrane and the released tumor antigen act together to effectively remodel the tumor immune microenvironment and promote the maturation of dendritic cells, polarization of macrophages to M1 type, infiltration of cytotoxic T cells and down-regulation of regulatory T cells, so that strong systematic anti-tumor immune response is stimulated; the anti-tumor efficiency is improved; and tumor migration is inhibited. The invention provides a referential strategy for developing a novel stimulus-responsive bionic nano-enzyme and applying the stimulus-responsive bionic nano-enzyme to tumor immunotherapy.

This invention provides a CD3-CTLA4-CD105 trispecific nanobody T-cell connector, its preparation method, and its applications. The T-cell connector comprises: a first functional domain capable of specifically binding to and effectively activating CD3 molecules on the surface of T cells; a second functional domain capable of specifically binding to the immune checkpoint CTLA-4 molecule; and a third functional domain capable of specifically binding to CD105 molecules on the surface of tumor neovascular endothelial cells. This invention also provides a method for preparing the T-cell connector and its applications. The T-cell connector provided by this invention can effectively activate the immune synapses and signaling connections of T cells, and by mediating the recruitment and activation of cytotoxic T cells to specifically target, infiltrate, and kill tumor cells, it has promising clinical application prospects in the field of tumor immunotherapy.

The invention discloses a compound for targeted inhibition of NQO1 / TrxR1 as well as a preparation method and application of the compound, and the compound is obtained by carrying out amidation reaction on 3-methyl-4, 5-dioxo-4, 5-dihydronaphthalene [1, 2-b] furan-2-carboxylic acid and (E)-1-(3-(4-(3-aminopropoxy)-3, 5-dimethoxyphenyl) acryloyl)-5, 6-dihydropyridine-2 (1H)-ketone. The compound can significantly inhibit proliferation of colorectal cancer cells, promote apoptosis and immunogenic death of the colorectal cancer cells, promote the killing effect of cytotoxic T cells on the colorectal cancer cells, reduce tumor immune escape and play an anti-tumor role.

The invention discloses a Brucella multi-epitope fusion protein, a vaccine, a preparation method and application, the Brucella multi-epitope fusion protein is designed based on a Brucella WbkC protein, a B cell epitope (LBL), a cytotoxic T cell epitope (CTL) and a helper T cell epitope (HTL) of the Brucella multi-epitope fusion protein are screened, and the Brucella multi-epitope fusion protein is prepared by connecting KK, AAY, GPGPG and GGGGS connecting peptides. A vaccine prepared from the fusion protein provided by the invention can provide better antigen-specific immune response than WbkC for immunizing mice. Therefore, the subunit fusion protein vaccine involved in the invention is expected to become a novel brucella vaccine, and has good application and development prospects.

This invention belongs to the field of immunotherapy and relates to a method for evaluating the immunogenicity of CAR molecules. The method utilizes dendritic cells (DCs) loaded with CAR molecule peptides, which are then induced to mature and co-cultured with T lymphocytes to obtain CAR-specific cytotoxic T cells. By restimulating the peptides, the IFN-γ secreted by the specific cytotoxic T cells is detected to determine the immunogenicity of the CAR molecule. Compared with existing methods, the detection method and platform described in this invention have advantages such as shorter detection time, higher convenience, less experimental cell consumption, and lower detection cost, and can be used for in vitro evaluation of the immunogenicity of CAR molecules.

Provided herein are peptide-based therapeutics that target POXP3 and methods of use thereof to decrease the immunosuppressive effects of Tregs and inhibit immune dysregulation, while sparring inhibition of activated cytotoxic T cells, for example, in the context of anti-tumor immune responses, autoimmunity, inflammatory conditions, etc.