116 results about "Treg cell" patented technology

The invention relates to the technical field of biology, in particular to a Treg cell amplification culture medium and a preparation method of Treg cells. According to the method for in-vitro amplification of the regulatory T cells (Treg) from peripheral blood, the amplification efficiency and purity of the Treg cells are improved, the culture cost is reduced, the culture period is shortened, and the problem of trophoblast cell residues in subsequent clinical application is solved.

A kit for detecting expression of AIRE and Treg in lymphatic tissue infected by EB virus comprises colloidal quantum well antibody conjugates, including a colloidal quantum well and protein AIRE and GITR conjugates and a colloidal quantum well and antibody CD25 and Foxp3 conjugates. The detection method comprises the following steps: (1) carrying out slicing treatment on a lymphatic tissue, and carrying out antigen repair by using an antigen repair liquid; (2) respectively adding colloidal quantum well proteins or antibodies coupled with different targets to dye the sections; (3) carrying out nucleus staining; and (4) collecting multi-channel fluorescence image information of the tissue slice, and judging expression levels and mutual relations of AIRE, Treg cells and dendritic cells in immune tolerance in combination with spatial positioning and intensity distribution of fluorescence signals of different channels. According to the invention, qualitative or quantitative multi-parameter and high-precision detection of the immune tolerance related cells in the lymph tissue is realized.

The invention discloses an immunomodulatory composition based on a cordycepin-selenium nano chelate and a preparation method thereof, and belongs to the technical field of biological medicines.The immunomodulatory composition is characterized in that 15-25 nm zero-valent selenium nano particles are chelated through hydroxyl of cordycepin and N7 site bidentate coordination, and a stable five-membered ring structure with the molar ratio is formed; the preparation method comprises the following steps: reducing sodium selenite in an inert atmosphere to generate selenium colloid, chelating the selenium colloid with a cordycepin ethanol solution, and carrying out ultrafiltration and freeze-drying to obtain the product. The invention aims to solve the problems of fuzzy structure, inconsistent batch, uncontrollable immunomodulatory function and the like caused by non-specific mixing in the prior art, and the composition can bidirectionally regulate and control IRF3 pathways, promote polarization of M2 type macrophages and proliferation of Treg cells, and has a clear immunomodulatory mechanism and excellent stability.

This invention relates to a pharmaceutical composition for treating autoimmune diseases. The pharmaceutical composition for treating autoimmune diseases comprises an antibody and an inhibitor, wherein the antibody includes at least one of an OX40 antibody and an OX40L antibody, and the inhibitor includes at least one of a Janus kinase inhibitor and a RORγt inhibitor. In the above-mentioned pharmaceutical composition for treating autoimmune diseases, the Janus kinase inhibitor and / or the RORγt inhibitor can inhibit the secretion of IL17A by Treg cells induced by OX40 antibody and / or OX40L antibody, thereby reducing IL17A-promoted pathological inflammation and improving the efficacy of OX40 antibody and / or OX40L antibody in treating autoimmune diseases.

A method of promoting T-cell function, comprising administering an effective amount of a compound of the present invention, including 2-hydroxybenzylamine, methyl-2-hydroxybenzylamine, or ethyl-2-hydroxybenzylamine; or a pharmaceutically acceptable salt thereof.

The present application relates to the medical technical field, especially to the application of FYB1 gene as a marker in preparation of gastric cancer diagnosis or prognosis judging reagent. The present application research finds that FYB1 gene is highly expressed in gastric cancer tissue and negatively correlated with the prognosis of patients, and can be used as a gastric cancer marker for gastric cancer detection and efficacy evaluation. In addition, FYB1 is positively correlated with the expression of Treg cell marker FOXP3 and co-localized in tissues, suggesting that FYB1 may promote gastric cancer tumor immune escape; the expression of FYB1 gene can significantly inhibit the proliferation, migration and invasion ability of gastric cancer cells, and inhibit tumor growth, indicating that FYB1 gene can be used as a gastric cancer treatment target and play an important role in the treatment of gastric cancer patients.

The present application relates to the technical field of biology, and discloses an anti-CCR8 antibody or an antigen binding fragment thereof, and a use thereof. The antibody can specifically bind to at least one epitope of CCR8, can also bind to Treg cells, has ADCC activity, and provides new possibilities for the treatment and / or prevention of cancer.

This invention belongs to the field of biomedical engineering technology, specifically the field of cell function detection technology, and relates to a method for evaluating the ability of mesenchymal stem cells (MSCs) to promote Treg cell proliferation. This method utilizes porous microcarriers to achieve three-dimensional cell distribution, employing low-speed rotation throughout the culture process to simulate the in vivo suspension microenvironment. A culture medium matching human physiological parameters is configured, with oxygen concentration adjusted to a hypoxic range of 1%-3% to simulate the microenvironment of inflammatory sites. Mononuclear cells with a purity of over 95% are obtained through magnetic bead sorting and co-cultured with MSCs for approximately 3 days, significantly shortening the culture period and reducing data deviation, thus achieving specific screening of MSCs with high immunomodulatory functions. By constructing a co-culture microenvironment that conforms to human physiological characteristics, this invention effectively improves detection sensitivity and repeatability, avoids interference from individual differences in peripheral blood mononuclear cells from different sources, and provides technical support for the quality control and clinical application of MSCs.

The invention relates to a method for screening and identifying metabolites and florae with a human immune regulation effect, which comprises the following steps: (1) establishing immune system humanized mice with multiple intestinal types, and analyzing the change of the florae, the metabolites and the immune system through intestinal flora sequencing, serum metabolome sequencing, flow cytometry and transcriptome sequencing; (2) determining the correlation and sequence between flora related metabolites and the change of the immune system through bioinformatics analysis; and (3) confirming the regulation and control relationship between the candidate metabolites and the immune subgroups in the step (2) through biological experiments. By means of the screening method, the chemical small molecule metabolites for regulating and controlling the human immune cells in the normal physiological state can be screened on a large scale, and the chemical small molecule metabolites can be developed into immunotherapy drugs or used as cell therapy drug culture system components. The screened propionic acid can promote cytotoxicity of T cells and CAR-T and secretion of related cytokines in the aspect of function regulation of the T cells, and the metabolite 2-hydroxybutyric acid is highly positively correlated with the Treg cells and can promote generation and functions of the Treg cells.

Disclosed are compositions and methods for preventing graft versus host disease (GVHD) or allograft rejection in subjects receiving donor cells. Also disclosed are methods enhancing regulatory T (Treg) cells for use in preventing GVHD. Also disclosed are methods of suppressing alloreactive donor cells in a subject receiving transplant donor cells that involves adoptive transfer of the treated Treg cells. Also disclosed are enhanced Treg cells produced by the disclosed methods that have been engineered to express chimeric antigen receptor (CAR) polypeptide cells.

The present disclosure provides a method of treating an autoimmune disease or inflammatory disease in an individual comprising administering to the individual a combination therapy. The combination therapy comprises a CD-2 binding molecule comprising a CD2-binding domain linked to an Fc domain and a composition comprising modified regulatory T (Treg) cells. The CD-2 binding molecule is administered first to precondition the individual for administration of the composition comprising the modified Treg cells.

This invention discloses a method for analyzing the distribution of plasmablasts and Treg cells based on tissue section images, belonging to the field of plasmablast and Treg cell distribution analysis technology. The method includes the following steps: labeling plasmablasts and Treg cells in tissue section images; statistically analyzing the distribution ratio of plasmablasts and Treg cells; calculating the mixed parameters of plasmablasts and Treg cells in the tissue section images; obtaining tissue section images with different prognostic effects as sample images and extracting mixed sample parameters; analyzing the correlation between mixed parameters and prognostic effects based on the mixed sample parameters; and determining whether the prognosis of mice is good based on the distribution of plasmablasts and Treg cells and the correlation. This invention addresses the problem that existing plasmablast and Treg cell distribution analysis techniques lack comprehensive and in-depth analysis of the distribution of plasmablasts and Treg cells, leading to biased assessments of prognostic effects.

The invention relates to the technical field of biological medicine, in particular to application of targeted DBC1 in treatment of systemic lupus erythematosus. The application for knocking out or inhibiting the expression of the DBC1 gene as shown in SEQ ID NO.1, or blocking or inhibiting the active function of the DBC1 protein as shown in SEQ ID NO.2 comprises the following applications: 1) inhibiting the transcription of STAT5 and inhibiting the activation of an STAT5 signal channel; 2) the differentiation of Treg cells is promoted, and the differentiation of Tfh and Th2 cells is inhibited; according to the application, DBC1 in DCs is inhibited or knocked out, STAT5 signal activity is lowered, then Treg differentiation is promoted, Tfh and Th2 differentiation is inhibited, and finally the SLE treatment effect is achieved.

The present invention provides methods of diagnosing, treating, and monitoring the progression of inflammatory bowel disease in a subject, including, for example, by monitoring RORγt+Th or RORγt+Treg cell levels and treating the subject accordingly.

The application discloses a lactobacillus rhamnosus capable of significantly increasing the number of enteric neurons and neuroglial cells and an application thereof, and belongs to the field of microorganisms.The lactobacillus rhamnosus CCFM1360 has good activity, certain acid and alkali resistance and adhesion, can significantly increase the number of enteric neurons and neuroglial cells, repair intestinal barrier function, increase the content of SCFAs in colon contents, increase the number of Treg cells in mesenteric lymph nodes, reduce the expression level of inflammatory factors in colon tissues, reduce the intestinal inflammation level, and relieve the weakened intestinal motility disorder.

The invention relates to the technical field of prevention and treatment of complications after organ transplantation, and discloses a preparation for preventing and treating diabetes mellitus after organ transplantation based on a Treg cell metabolic regulation function and application, the preparation takes repair or enhancement of the Treg cell metabolic regulation function as a core action mechanism, and comprises at least one active component, according to the PTDM prevention and treatment preparation based on the Treg cell metabolic regulation function and the application, the preparation contains IL-2 / anti-CD3 / CD28 beads, FKBP12siRNA, a PPAR-gamma agonist, SOCS-3siRNA and other active ingredients, and the active ingredients are matched with pharmaceutical auxiliary materials to be prepared into an injection or a freeze-dried powder injection; the preparation is suitable for PTDM high-risk recipients using CNI after kidney / heart transplantation, has a single drug and combination scheme, can also amplify Treg cells in vitro for transfusion to assist intervention, can realize'immune tolerance-metabolic regulation 'double-effect synergy, accurately target PTDM key pathways, adapt to multiple transplantation types, and can be combined with CPB for blood perfusion to synergistically reduce PTDM and AKI risks, reduce non-target injury and improve the curative effect of the PTDM. The life quality of a recipient is improved, the medical burden is reduced, and the blank of PTDM immunotherapy is filled.

The invention provides a preparation method and application of an anti-IL-11 antibody modified Treg cell, and belongs to the technical field of genetic engineering.The preparation method of the anti-IL-11 antibody modified Treg cell comprises the steps that after the Treg cell and umbilical cord blood pluripotent stem cells are co-cultured, the Treg cell is separated and recycled, an anti-IL-11 antibody is adopted for modification, and the anti-IL-11 antibody modified Treg cell is obtained; the nucleotide sequence of the anti-IL-11 antibody is as shown in SEQ ID NO. 2 in the sequence table. In the co-culture process, stem cells are used for providing an immune microenvironment, promoting Treg cell amplification and enhancing the inhibition ability of Treg cells, and obtaining the specific recognition ability of pancreas islet beta cell antigens, so that autoimmune attacks are inhibited more accurately; the nucleotide sequences of the heavy chain and the light chain of the anti-IL-11 antibody are optimized, and the anti-IL-11 antibody has higher efficacy in treatment of diabetic mice.

To provide a population of cord blood-derived regulatory T cells expanded ex vivo. To provide a method for producing a population of cord blood-derived regulatory T cells expanded ex vivo, and a method for using the same.SOLUTION: Provided is a population of human Treg cells comprising at least about 1 * 10 8 human Treg cells, wherein (i) ≥ 60% are CD4 + CD25 + and (ii) ≤ 10% are CD4 - CD8 +, wherein said human Treg cells are immunosuppressive.SELECTED DRAWING: Figure 1

The invention belongs to the technical field of biological medicine, provides a mustard gas immunotoxicity evaluation method based on Foxp3 promoter methylation, and evaluates the application effect of the Foxp3 promoter methylation level in mustard gas immunotoxicity evaluation in combination with in-vitro cell experiments and in-vivo animal experiments. Results show that Treg cell deficiency is a main reason for tissue damage and inflammation caused by mustard gas poisoning, cell fate and functions of the Treg cell deficiency are mainly regulated and controlled by Foxp3 transcription factors, mustard gas can cause increase of the DNA methylation level of Foxp3 gene loci, DNA hypermethylation of Foxp3 promoters is crucial to Treg cell differentiation inhibition, Th17 / Treg imbalance and systemic inflammation caused by mustard gas exposure, and the Treg cell deficiency is a main reason for tissue damage and inflammation caused by mustard gas poisoning. The methylation level of the Foxp3 promoter can be used as a marker of a mustard gas immunotoxicity evaluation method.

Provided are recombinant cytokine receptors that comprise an IL-2 intracellular domain and an extracellular domain that binds to a cytokine other than IL-2. Also provided herein are Treg cell comprising recombinant cytokine receptors and methods of use.

The application belongs to the technical field of biological medicine, and particularly relates to application of CDC37 protein in preparation of Treg cell dysregulation disease treatment product. The application obtains a CDC37 protein with immunoregulatory function and high expression through mass spectrum analysis and bioinformatics analysis on proteins of lung stage child worms of Japanese blood flukes. The amino acid sequence of the CDC37 protein is shown as SEQ ID NO. 1, and the nucleotide sequence of the gene coding the CDC37 protein is shown as SEQ ID NO. 2. Experimental results show that the CDC37 protein can realize the effect of non-hormone-dependent long-acting relief of Treg cell dysregulation diseases by inducing Treg cell expansion, inhibiting Th2 response and reducing airway hyperresponsiveness, and can be used for preparation of Treg cell dysregulation disease treatment product.

The application discloses an anti-TIGIT humanized antibody or an antigen binding fragment thereof and application thereof. The antibody or the antigen binding fragment thereof has good binding activity and blocking activity, has a remarkable anti-tumor effect, effectively prolongs the survival period of a mouse, remarkably reduces the proportion of Treg cells in healthy human PBMCs and tumor infiltrating lymphocytes, has good stability and good drug property, and can be widely used for preventing or treating immune diseases or tumor related diseases.

The invention belongs to the field of biological medicine, and relates to a preparation method and application of a metabolic syndrome animal model. The invention provides a preparation method and application of a metabolic syndrome animal model, the preparation method comprises the step of modifying genes in immune cells in an animal body, and the modification reduces or eliminates the function or level of Abhd5 in Treg cells.

The invention belongs to the technical field of cell biology, and particularly relates to a culture medium for amplifying Treg cells, a culture method and application. The culture medium comprises an activation culture medium and an amplification culture medium, wherein the activated culture medium is prepared from a serum-free culture medium, IL-2 (Interleukin-2), TGF (Transforming Growth Factor)-beta (beta), rapamycin, IL-27 (Interleukin-27), retinoic acid and Anti-Human CD3 / CD28 beads; the amplification culture medium comprises a serum-free culture medium, IL-2, rapamycin and IL-27. According to the invention, the culture medium combination with a specific formula and proportion is adopted, and the synergistic effect of the IL-2, the TGF-beta, the rapamycin, the IL-27, the retinoic acid and the Anti-Human CD3 / CD28 beads is utilized, so that the amplification multiple and the immunosuppression capability of the Treg cells are remarkably improved. The invention provides a more efficient and safer technical scheme for clinical application of Treg cell therapy.

The present disclosure provides for IL2 engrafted into the CDR sequences of an antibody having preferred therapeutic profiles over molecules known and used in the clinic. In particular, the provided antibody cytokine engrafted protein compositions increase or maintain CD8+ T effector cells while reducing the activity of Treg cells. Additionally, provided compositions convey improved half-life, stability and produceability over recombinant human IL2 formulations such as Proleukin®.

The present invention provides a composition comprising dendritic cells loaded with hHsp60sp, which dendritic cells are from a subject and have been fixed with paraformaldehyde (PFA). The subject may suffer from an autoimmune disease. Also provided are a method for preparing the composition; recombinant human cells comprising a heterologous gene encoding a fusion protein of HLA-E and hHsp60sp or B7sp, and expressing the fusion protein on the surface of the cells; a method for determining a percentage of maximum inhibition of testing the function of the HLA-E restricted CD8+ Treg cells from a subject, determining whether HLA-E restricted CD8+ Treg cells freshly isolated from a subject are defective, or determining whether defective HLA-E restricted CD8+ Treg cells from a subject are correctable; and a method for correcting defective HLA-E restricted CD8+ Treg cells, treating type 1 diabetes (T1D), or treating multiple sclerosis (MS).

It was found that bacteria belonging to the genus Clostridium induce accumulation of regulatory T cells (Treg cells) in the colon. Moreover, the present inventors found that regulatory T cells (Treg cells) induced by from these bacteria suppressed proliferation of effector T-cells. From these findings, the present inventors found that the use of bacteria belonging to the genus Clostridium or a physiologically active substance derived therefrom made it possible to induce proliferation or accumulation of regulatory T cells (Treg cells), and further to suppress immune functions.

The present disclosure relates to a Treg-cell-targeting IL12 fusion protein, a corresponding nucleic acid molecule, vector, cell and pharmaceutical composition, a corresponding production method, a corresponding method for treating tumors, and the pharmaceutical use. Relative to a systemic immune system, the Treg-cell-targeting IL12 fusion protein of the present disclosure selectively activates the tumor microenvironment, especially inducing the secretion of IFNg by intratumoral Treg cells, thereby reducing or eliminating the immunosuppressive effect thereof.

This invention relates to the field of antibody drug technology, and more particularly to TNFR2 antibodies and their applications. The TNFR2 antibody of this invention binds specifically to human TNFR2 and monkey TNFR2 with high affinity, and specifically blocks the binding of the ligand TNFα to TNFR2. It can also inhibit the proliferation of Treg cells in vitro and promote the expansion of Teff cells. In vivo experiments in mice show that this molecule significantly inhibits tumor growth. Its antitumor effect is mainly achieved by selectively inhibiting the activity of TNFR2 in immunosuppressive cells (Tregs), thereby weakening the inhibition of T effector cells by Tregs, promoting the activation and expansion of T effector cells, alleviating the immunosuppressive microenvironment, and thus enhancing the antitumor immune response.