24 results about "Immuno modulation" patented technology

The present disclosure pertains to the recognition that immune responses mediated by CpG oligonucleotides can be affected by the stereochemistry of modified internucleotidic linkages such as phosphorothioates. In some embodiments, the present disclosure relates to chirally controlled CpG oligonucleotide compositions comprising CpG oligonucleotides comprising multiple modified internucleotidic linkages such as phosphorothioate linkages, wherein the oligonucleotides comprise one or more CpG region motifs having defined stereochemistry patterns of chiral internucleotidic linkages. In some embodiments, CpG oligonucleotides comprising one or more CpG region motifs are capable of agonizing an immune response. In some embodiments, CpG oligonucleotides comprising one or more CpG region motifs are antagonistic. Methods for making and using chirally controlled CpG oligonucleotide compositions are also described. In some embodiments, no immune modulation is desired, and the present disclosure provides methods of identifying chirally controlled oligonucleotide compositions which have decreased immune modulation.

The present disclosure provides triptolide conjugates, methods of making such compounds, pharmaceutical compositions and medicaments comprising such compounds, and methods of using such compounds to treat conditions / diseases, such as those related to cancer, immune modulation, and / or inflammation.

The present disclosure provides a peptide-major histocompatibility complex (pMHC) polypeptide comprising a peptide epitope and class I MHC polypeptides. The present disclosure provides fusion molecules comprising a pMHC polypeptide and a heterologous fusion partner. The present disclosure provides single-chain T-cell modulatory polypeptides that comprise a pMHC polypeptide, one or more immunomodulatory polypeptide, and an immunoglobulin (Ig) Fc or a non-Ig scaffold. A TMP is useful for modulating the activity of a T cell, and for modulating an immune response in an individual.

The present disclosure relates to engineered bacteria, compositions and methods for immune modulation, specifically Bacteroides ovatus strains locked in a defined orientation at a genomic locus undergoing phase variation. The resulting "ON" and "OFF" mutants showed distinct immunomodulatory effects in vitro and in vivo, including differential cytokine secretion, regulatory T cell induction, and antitumor activity. These engineered strains offer a novel platform for modulating immune responses in cancer, autoimmune, and inflammatory diseases.

The invention relates to the technical field of targeted protein degradation, and discloses a probiotic for targeted degradation of rice-derived allergenic protein and application, the probiotic is a new sphingomonas strain, the probiotic secretes an extracellular protease compound in the fermentation process, the rice allergenic protein with the molecular weight of 14 kDa and 26 kDa is specifically degraded, the degradation rate is larger than 90%, and the probiotic can be used for degrading the rice-derived allergenic protein in a targeted mode. By introducing a targeted degradation technology, in the process of intervening rice sensitization protein by probiotics, a specifically secreted protease compound is utilized to directly decompose key antigen epitopes of the sensitization protein and reduce immunogenicity of the sensitization protein, and meanwhile, by regulating intestinal immune balance, inhibiting excessive Th2-type immune response and enhancing regulatory T cell activity, the rice sensitization protein can be effectively degraded. The method can be used for blocking the allergy cascade reaction, realizing the dual synergy of high-efficiency elimination and immune tolerance of sensitization protein, breaking through the limitation that traditional probiotics only depend on indirect immune regulation, and improving the desensitization efficiency and safety.

A combination therapeutic strategy employs multiple oncolytic viruses (OVs), grouped and administered based on their virological properties, tumor selectivity, and distinct antigen profiles, to treat malignant tumors. Representative groupings may include members of flaviviruses, each contributing distinct immune modulation and the same modes of tumor cell killing. A predefined treatment schedule involves sequential or concurrent administration of antigenically diverse OVs in multiple cycles, reducing cross-neutralization and sustaining cytolytic pressure on tumors. A pre-characterized OV panel, comprising members from a virus family, RNA and DNA viruses, both wild-type and genetically engineered, serves as a flexible resource for customizing treatment regimens by tumor type, immune landscape, and therapeutic goals. This platform establishes a rational framework for combination OV therapy with improved durability, safety, and clinical effectiveness.

Multi-specific, optionally multi-valent, antibodies comprising at least one antigen binding moiety in Fv format. Also provided herein are methods for making such multi-specific antibodies and uses thereof for modulating immune responses and treating diseases such as cancer.

In the present invention, the inventors reveal that noncoding RNA, a known source of noncanonical peptides (also called dark matter) and tumour-specific antigens, can shape the precancer immune contexture and are associated with polyp and cancer risk. Through the multimodal characterisation of a unique dataset of 135 well-annotated cancer and precancer lesions from patients developing polyps at low and high frequency, the inventors identified high expression of noncoding RNAs, as a major differentiator of polyp development rate. Noncoding RNAs were also associated with increased immunogenicity associated with increased mature tertiary lymphoid structures within the microenvironment of pre-cancer lesion, higher quantity and quality of adaptive immune cells, including B- and T-cells. Thus, the inventors propose that early carcinogenesis is shaped by noncoding RNA expression and immune microenvironment. These compelling findings reveal potential early biomarkers and targets for prophylactic immune modulation approaches in individuals at high risk of developing colorectal cancer.

The invention discloses an immunoregulation method based on amniotic mesenchymal stem cells, and relates to the technical field of immunoregulation, and the method comprises the following steps: establishing an acoustic simulation model of a subcellular structure, predicting the sensitive frequency range of mitochondria and endoplasmic reticulum in amniotic mesenchymal stem cells based on the simulation model, and a safe frequency interval in which subcellular resonance is not caused is determined. According to the method, the subcellular sensitive frequency is predicted by constructing the acoustic simulation model, the resonance risk is avoided in combination with multi-frequency standing waves, real-time monitoring and a self-adaptive regulation and control mechanism are integrated, and it is guaranteed that the organelle function is stable. After separation, function detection and model feedback optimization are performed to form a'modeling-monitoring-regulation-verification-feedback 'closed-loop system, so that the survival rate and the immune regulation function of the amniotic mesenchymal stem cells are remarkably improved, and the process stability and the clinical availability are enhanced.

Certain embodiments provide RNA nanostructure (e.g., comprising one single-stranded RNA (ssRNA) molecule, wherein the RNA nanostructure comprises at least one paranemic cohesion crossover), as well as compositions and methods of use thereof. In certain embodiments, such RNA nanostructures are immuno-modulatory (e.g., immuno-stimulatory).

Disclosed are methods for treating a cancer and / or modulating immune CD4+ T cell mediated therapies comprising administering to a subject a fucose. In one aspect, disclosed herein are methods of modulating major histocompatibility complex II human lymphocyte antigen (HLA)-DRB 1 expression on the surface of a cell comprising contacting the cell with an agent that modulates the amount of fucosylation on the cell; wherein an increase in fucosylation increases surface expression of HLA-DRB 1; and wherein a decrease in fucosylation decreases the surface expression of HLA-DRB 1.

The invention discloses an application of mitochondrial acid 5 in preparation of a product for enhancing the immunomodulatory ability of regulatory B cells, and provides a method for enhancing the immunomodulatory ability of the regulatory B cells. The regulatory B cells are pretreated by the mitochondrial acid 5, so that the expression of interleukin-10 in the regulatory B cells can be promoted, and the treatment effect of the regulatory B cells on autoimmune diseases, chronic inflammatory diseases and / or organ transplantation rejection can be enhanced; therefore, the invention also claims the protection of the application of mitochondrial acid 5 in the preparation of a synergist for a medicament for treating autoimmune diseases, chronic inflammatory diseases and / or organ transplant rejection. The invention develops a safe, efficient and specific method for promoting B lymphocyte to differentiate to functional Bregs and secrete interleukin-10, and the method can effectively inhibit over-active immune response and avoid self tissue damage.

The present disclosure provides a T-cell modulatory multimeric polypeptide (TMMP) comprising at least one heterodimer, where the heterodimer comprises first and second polypeptide chains and where the heterodimer includes an NKG2 peptide, an HLA-E heavy chain polypeptide, a beta-2 microglobulin polypeptide, and an immunoglobulin Fc polypeptide. The heterodimer can also include an immunomodulatory polypeptide and / or a cancer-targeting polypeptide. The TMMPs are useful in methods of modulating an immune response, which methods are also provided.

In the present invention, the inventors reveal that noncoding RNA, a known source of noncanonical peptides (also called dark matter) and tumour-specific antigens, can shape the precancer immune contexture and are associated with polyp and cancer risk. Through the multimodal characterisation of a unique dataset of 135 well-annotated cancer and precancer lesions from patients developing polyps at low and high frequency, the inventors identified high expression of noncoding RNAs, as a major differentiator of polyp development rate. Noncoding RNAs were also associated with increased immunogenicity associated with increased mature tertiary lymphoid structures within the microenvironment of pre-cancer lesion, higher quantity and quality of adaptive immune cells, including B- and T-cells. Thus, the inventors propose that early carcinogenesis is shaped by noncoding RNA expression and immune microenvironment. These compelling findings reveal potential targets for immune modulation approaches in individuals at high risk of developing colorectal cancer. More particularly, the inventors identified dark antigens (i.e. peptides) that can be used in vaccines for the treatment of cancer, in particular, the prophylactic treatment of cancer.

Certain embodiments provide RNA nanostructure (e.g., comprising one single-stranded RNA (ssRNA) molecule, wherein the RNA nanostructure comprises at least one paranemic cohesion crossover), as well as compositions and methods of use thereof. In certain embodiments, such RNA nanostructures are immuno-modulatory (e.g., immuno-stimulatory).

The present disclosure provides a peptide-major histocompatibility complex (pMHC) polypeptide comprising a KRAS peptide and class I MHC polypeptides. The present disclosure provides fusion molecules comprising a pMHC polypeptide and a heterologous fusion partner. The present disclosure provides single-chain T-cell modulatory polypeptides that comprise a pMHC polypeptide, one or more immunomodulatory polypeptide, and an immunoglobulin (Ig) Fc or a non-Ig scaffold. A TMP is useful for modulating the activity of a T cell, for modulating an immune response in an individual, and / or for treating an individual who has a KRAS-associated cancer.

Aspects of the present disclosure include methods for modulating macrophage activity. Methods according to certain embodiments include contacting a macrophage with a mannose receptor (CD206) binding agent in a manner sufficient to modulate activity of the macrophage. Methods for converting a phenotype of a macrophage from an M2 phenotype to an M1 phenotype are also provided. Methods for inhibiting growth of a CD206-expressing cell as well as methods for treating a subject for a neoplastic condition (e.g., cancer) or a condition associated with chronic inflammation are described. Immuno-modulating peptides suitable for use in the subject methods are also presented.

This invention provides an antigenic polypeptide for anti-tumor immune regulation, a screening method thereof, and its application. The antigenic polypeptide is derived from BCG, and its amino acid sequence is shown in SEQ ID NO. 1-8. The screening method combines immunomass spectrometry detection with antigenicity prediction. The antigenic polypeptide can activate CD8. + T cells regulate the tumor immune microenvironment and induce intratumoral CD8. + The increase in T and DC2.4 cells, coupled with the enhanced induction effect of the peptide delivered via iodized oil, provides a strong basis for the screening method of this invention. This invention provides technical support for the development of novel BCG antitumor agents, enriches the application of BCG in antitumor therapy, and offers insights for the development of tumor immunotherapy materials.

To provide biomarkers for predicting tumor response to and toxicity of immunotherapy.SOLUTION: The invention is directed to biomarkers for predicting a patient's response, both therapeutic and toxic, to immunotherapy. The invention is based, in part, on the discovery that cancer patients carrying one or more specified mutations in their genome may respond to treatment with an immune modulating agent more effectively than other cancer patients, for example, patients homozygous for the wild-type allele. The invention is also based, in part, on the discovery that cancer patients carrying one or more specified mutations in their genome may respond to treatment with an immune modulating agent less effectively than other patients, for example, cancer patients homozygous for the wild-type allele.SELECTED DRAWING: None

The utility model relates to the technical field of biological cells, in particular to an immunomodulatory cell scraping component which is used for adjusting the flatness of equipment through an adjusting device, preventing culture solution in a culture dish from being non-uniformly distributed to influence the scraping operation of normal immune cells, adapting to culture dishes with different sizes through a fixing device, and improving the scraping efficiency. A culture dish is fixed in an auxiliary manner, and cells in the culture dish are scraped through a scraping device, so that the practicability of the device is improved; comprising an adjusting device, a fixing device and a scraping device, the fixing device is installed on the adjusting device, and the scraping device is installed on the adjusting device.

This invention discloses a method for preparing regulatory T cell-derived functionalized reconstructed vesicles, comprising the following steps: obtaining and expanding high-purity human Treg cells; resuspending the Treg cells in buffer solution, adjusting the density, and pre-treating with ultrasound; then, using a liposome extruder driven by a constant-speed injection pump, sequentially passing the Treg cell suspension through polycarbonate filter membranes with pore sizes of 10 μm, 5 μm, 1 μm, and 0.4 μm at different pressures for stepwise reconstruction; subsequently, enriching and purifying the reconstructed vesicles by high-speed centrifugation, graded filtration, and ultracentrifugation. The Treg-RVs prepared by this invention have uniform particle size, high concentration, and completely retain the core immunomodulatory functions of parental Treg cells, effectively inhibiting T cell proliferation.

This invention discloses the use of donkey-hide gelatin in the preparation of products for treating postmenopausal osteoporosis, belonging to the field of new pharmaceutical applications of donkey-hide gelatin. The use of donkey-hide gelatin in the preparation of products for treating postmenopausal osteoporosis utilizes a mechanism of action that regulates immune cells to mediate bone immune balance, thus treating osteoporosis. This invention reveals for the first time a novel mechanism by which donkey-hide gelatin regulates immune cells to mediate bone immune balance. This mechanism endows traditional donkey-hide gelatin with entirely new pharmaceutical value, exceeding expectations based on its traditional description as "strengthening muscles and bones." It indicates that donkey-hide gelatin can be used to prepare drugs or health products for treating postmenopausal osteoporosis, and is particularly suitable for the development of anti-osteoporosis preparations based on immune modulation mechanisms.

The invention relates to an application of overexpressed NLRC3 in treating right ventricular (RV) remodeling caused by pulmonary arterial hypertension (PH), in particular to an AAV vector of overexpressed NLRC3 by adopting myocardial in-situ injection and / or tracheal instillation, or Treg cells of in-vitro overexpressed NLRC3 by adopting adoptive transfer. Verification shows that in the RV reconstruction process, the number of Treg cells is rich, and the Treg cells are crucial to reduction of harmful effects of RV reconstruction; the RV Treg cells show remarkable regional heterogeneity and compensatory characteristics, which are related to the NLRC3 level, mainly because the inactivation of the NLRC3-JAK2 / STAT4 pathway promotes the down-regulation of the Th1-Treg cells and weakens the immunosuppression function of the RV Treg cells; the RV remodeling can be aggravated by NLRC3 defects, RV dysfunction and failure are caused, RV remodeling is remarkably inhibited by the NLRC3 overexpressed Treg cells, and a new treatment strategy is provided for precise immunoregulation of RV remodeling caused by PH.