44 results about "Autoimmune responses" patented technology

The present disclosure provides inter alia, molecules comprising an autoantibody-binding domain and at least one modified Fc domain. The present disclosure also provides methods and compositions that allow for selective depletion and / or neutralization of pathogenic autoantibodies.

The present disclosure provides inter alia, molecules comprising an autoantibody-binding domain and at least one modified Fc domain. The present disclosure also provides methods and compositions that allow for selective depletion and / or neutralization of pathogenic autoantibodies.

The present invention relates to tetrahydrobenzo-isoquinoline sulfonamides derivatives of formula (I), processes for preparing them, pharmaceutical compositions containing them and their use in treating disorders caused by IgE (such as allergic responses, non-allergic mast cell responses or certain autoimmune responses), and in particular disorders caused by the interaction of IgE with the FIERI receptor.

The invention belongs to the field of new application of medicines, and particularly relates to application of SIRT4-IN-1 in preparation of medicines for treating autoimmune diseases. It is found for the first time that SIRT4-IN-1 reduces the activation degree of immune response induced by HSV-1 virus infection by up-regulating acetylation modification of cGAS, inhibits abnormal activation of immune response in Trex1 deficient mouse cells and peripheral blood mononuclear cells of systemic lupus erythematosus patients, and improves abnormal activation of autoimmune response. The invention provides a new candidate drug for clinical treatment of systemic lupus erythematosus.

The present disclosure describes methods of specifically modulating the activity and / or number of regulatory T (Treg) cells within a tumor in a subject. Such methods may be used to reduce the number of regulatory T cells within a tumor in a subject, as well as to inhibit tumor growth in a subject with cancer without eliciting an autoimmune response. This method relies on the inhibition of CD36 or PPARbeta.

The invention belongs to the field of biological medicine, and discloses a membrane binding type IL7 fusion protein, an engineered immune cell for expressing the membrane binding type IL7 fusion protein and application of the membrane binding type IL7 fusion protein. The fusion protein comprises an IL7 region and a transmembrane domain and can be expressed on a cell membrane, the tumor cell killing ability and the T cell survival ability of T cells expressing the fusion protein are both enhanced, and the aims of improving the tumor immune cell treatment effect and reducing the toxic and side effects are achieved. Particularly, the IL7 fusion protein anchors and expresses IL7 on the surface of a cell through transmembrane domains such as CD80 or PD-L1 and the like, so that (1) immune cells can be accurately regulated and controlled, the possibility that an excessive IL7 signal possibly causes autoimmune response or aggravates CRS is reduced, and the safety of the IL7 to immune cells such as T cells and the like is enhanced; (2) the half-life period of IL7 is prolonged, and the anti-tumor effect of adoptive immune cells is enhanced; and (3) the transmembrane fragment is linked with the IL7 through a hinge region of the flexible linker G4S, CD80 or PD-L1, so that the flexibility of the IL7 is enhanced, and the proliferation and killing functions of the IL7 on T cells are enhanced.

This invention relates to the field of traditional Chinese medicine and natural medicines, and discloses a traditional Chinese medicine composition for treating thyroiditis, nodular goiter, and thyroid nodules, as well as its preparation method and application. The traditional Chinese medicine composition is made from raw materials in parts by weight of 1-30 parts of Prunella vulgaris, 1-30 parts of Taraxacum mongolicum, 1-30 parts of Hordeum vulgare malt, 1-20 parts of Citrus reticulata peel, 1-24 parts of Crataegus pinnatifida, and 1-24 parts of Raphanus sativus seed. It can not only significantly reduce serum TgAb and TPOAb antibody levels, inhibiting the attack of autoimmune response on the thyroid gland from the source, but also effectively reduce lymphocyte infiltration, repair damaged thyroid follicular structure and restore colloid content, thereby reversing immune damage and tissue destruction of the thyroid gland, reducing thyroid nodules, and solving the problems of existing treatments for thyroiditis, nodular goiter, and thyroid nodules that cannot reverse immune damage to the thyroid gland, destruction of follicular structure, and tissue fibrosis.

Methods for treating immune diseases, specifically methods for the prevention and / or inhibition of autoimmune response or overactive immune response, comprising administering to the subject an effective amount of a compound of formula I, X or XI, or a pharmaceutically acceptable salt or solvate thereof. Methods for the prevention and / or inhibition of autoimmune disease, allergic disease or immune-mediated inflammatory disease, comprising administering to the subject an effective amount of a compound of formula I, X or XI, or a pharmaceutically acceptable salt or solvate thereof.

The present disclosure provides inter alia, molecules comprising an autoantibody-binding domain and at least one modified Fc domain. The present disclosure also provides methods and compositions that allow for selective depletion and / or neutralization of pathogenic autoantibodies.

The invention discloses a breeding method for increasing the yield of broom corn millet, and relates to the technical field of seed seedling cultivation, and the breeding method comprises the following steps: S1, seed memory induction environment construction and seed pretreatment, S2, seed memory related marking and screening, S3, directional memory consolidation and breeding, and S4, memory verification and optimization adjustment. According to the method, valley intercropping is selected, so that the germination rate and the seedling survival rate of seed offspring in a simulated drought environment are greatly improved; seed storage and memory strengthening utilize a special environment, so that the stress-resistant gene expression quantity is improved, and the yield loss is reduced; based on a marking technology of plant autoimmune response, microbial fermentation enzyme is adopted to prepare a marking compound, the marking accuracy is improved, seed physiological changes are associated, biocenosis screening is set through a specific environment and obstacles, the disease incidence rate is reduced, and the insect attracting capacity is enhanced; environmental relay induction, hybridization and mutation breeding consolidate and expand seed memory advantages from different aspects, and improve yield and stress resistance.

Systems and methods are provided that assess eye movement in multiple sclerosis (MS) patients receiving different drugs (e.g., dimethyl fumarate, fingolimod, clababine, ofarmumab) or treatments that (a) alleviate inflammation that may cause a symptom of multiple sclerosis and prevent nerve injury that may cause a symptom of multiple sclerosis); (b) testing sphingosine-1-phosphate receptor modulators that chelate lymphocytes in the lymphocyte nodes, preventing them from causing an autoimmune response); (c) checking for immunosuppressants acting on the lymphocyte pathway); and (d) analyzing the effect of the monoclonal antibody in inhibiting activation of lymphocyte B.

A method of treating or ameliorating an inflammatory autoimmune response, comprising administering to a patient in need there of an effective gamma-ketoaldehyde scavenging amount of a gamma-ketoaldehyde scavenging compound.

The invention provides a fusion protein, a nucleic acid construct encoding the fusion protein and regulatory T-cells (Treg) expressing the fusion protein for use in the treatment of inflammatory bowel disease, wherein the fusion protein is a chimeric antigen receptor (CAR) having a single chain variable fragment (scFv) domain specific for being activated by the location of inflammatory bowel disease, especially binding to one of meprin 1α (MEP1A) and cadherin 17 (CDH17), a transmembrane domain and at least one intracellular signalling domain. The scFv domains specific for MEP1A or CDH17 have been found to selectively bind to intestine afflicted by inflammatory bowel disease and to activate suppressive activity in Treg expressing the CAR at the location of inflammatory bowel disease. Specifically, the invention provides a CAR for use in the treatment of an immune response, e.g. in the treatment of an autoimmune response, which is directed against MEP1A or directed against CDH17.

The invention relates to the technical field of animal models, and discloses a construction method of a thyroid-associated ophthalmopathy animal model, which comprises the following steps: extracting retroocular soft tissue homogenate of mice, mixing the retroocular soft tissue homogenate with a complete Freund's adjuvant to obtain an emulsifier, carrying out multi-point injection on the mice by using the emulsifier, inducing the mice to generate autoimmune response, and constructing the thyroid-associated ophthalmopathy animal model. And generating the thyroid-associated eye disease rat model. Pathological characteristics of the animal model obtained through construction better conform to clinical pathological characteristics, that is, eye pathological characteristics are obvious, and changes of TSH, TRAb, FT3 and FT4 in serum and pathological changes of eye soft tissue and thyroid tissue conform to pathological changes of thyroid-related eye diseases.

Disclosed herein are ex vivo activated and culture-expanded regulatory cells or effector cells that have been stimulated with IL- 2 and IL-33 or variants thereof, IL-2 and IL- 33 fusion proteins (IL-233) or variants thereof for the prevention or suppression of immune reactions in a host, including autoimmune responses. The resulting ex vivo culture-expanded regulatory cells can be used for therapeutic uses, including the preventing, suppressing, blocking or inhibiting rejection of transplanted tissue in a human or other animal host, or protecting against graft vs host disease (GVHD). The resulting ex vivo culture-expanded effector cells can be used for anti-cancer / anti-tumor therapeutic uses. Also provided are therapeutic and immunosuppressive methods utilizing the ex vivo culture-expanded regulatory cells or effector cells for human treatment.

The present invention relates to a composition for preventing or treating Behcet's disease and rheumatoid arthritis, the composition comprising a peptide or a mixture thereof as an active ingredient. More specifically, it was found that intraperitoneal injection of P1 to P5 peptides or a mixture thereof or application as a skin external preparation to a mouse animal model having Behcet's disease caused by an autoimmune response can improve skin ulceration and skin inflammation in the Behcet's disease mouse model, and an improvement effect on arthritis of a rheumatoid arthritis animal model was also observed. Accordingly, a composition comprising P1 to P5 peptides or a mixture thereof as an active ingredient can be provided as a medicament for Behcet's disease and rheumatoid arthritis.

The application relates to the field of biological medicine, and particularly to application of miR-3158-3p in preparation of a drug for treating myasthenia gravis and a pharmaceutical composition. The drug exerts a therapeutic effect through double mechanisms of immunoregulation and nerve protection. The immunoregulation mechanism is that the drug promotes differentiation of Treg cells and enhances the immunoregulation function of the Treg cells by supplementing miR-3158-3p, simultaneously inhibits excessive activation of Th17 cells, corrects an immune tolerance imbalance state in a myasthenia gravis patient, and inhibits abnormal autoimmune responses of the body. The nerve protection mechanism is that the drug can improve biophysical properties of a neuron cell membrane, significantly improves membrane fluidity of the neuron cell membrane, and optimizes neurotransmitter recovery function in an inter-synaptic gap, thereby providing a structural basis for repairing signal transmission disorders of neuromuscular junctions and improving nerve damage of myasthenia gravis.

The present invention relates to dihydrocyclopenta-isoquinoline-sulfonamide derivatives of formula (I), processes for preparing them, pharmaceutical compositions containing them and their use in treating disorders caused by IgE (such as allergic responses, non-allergic mast cell responses or certain autoimmune responses), and in particular disorders caused by the interaction of IgE with the FcεRI receptor.

The invention discloses construction and application of a novel humanized locus systemic lupus erythematosus mouse model, and provides a brand-new humanized systemic lupus erythematosus mouse model for the first time, and a spontaneous lupus mouse Fas / lpr is hybridized with an hCD38 humanized locus mouse, so that the mouse model is obtained. According to the present invention, the stable mouse model carrying the humanized site (hCD38) and the lupus mutant gene (lpr) is obtained, the mouse model can well simulate the typical autoimmune response of the SLE, and the invention provides the SLE treatment related target drug research model and the disease mechanism research model for the field, and the method can be directly used for verifying the effectiveness of the medicine designed aiming at the hCD38 target spot.

The present invention relates to the area of improved anti-IgE antibodies and antigen binding agents, and compositions thereof, which target IgE, for instance: for use in treating disorders caused by IgE (such as allergic responses, or certain autoimmune responses); and, in particular, disorders caused by the interaction of IgE with the FcεRI receptor. In particular, this invention relates to improved anti-IgE antibodies and antigen binding agents related to novel mutants of omalizumab (Xolair®). The improved anti-IgE antibodies and antigen binding agents of the invention may have improved affinity for IgE and / or an improved interaction with the Cε2 domain of IgE and / or an improved modified epitope on IgE (for instance further involving the Cε2 domain of IgE) and / or the ability to disassociate IgE from the FcεRI receptor for instance at pharmaceutically-relevant concentrations. In one aspect, improved or novel treatments for IgE mediated disorders are disclosed in which IgE is targeted (for instance free IgE and / or IgE complexed with the FcεRI receptor).

The present invention relates to a detection kit for B cells and high endothelial venules in the immune microenvironment of thymus tissue, comprising quantum dot-labeled antibody CD19, quantum dot-labeled antibody CD1d, quantum dot-labeled CD31 and quantum dot-labeled PNad. After the specific antibody coupled with the quantum dot is specifically combined with the antigen on the B cell and high endothelial venule on the tissue section sample, the quantum dot can be used to quantify or locate the B cell and high endothelial venule. Instead of the traditional multicolor immunofluorescence technology, the method of directly carrying specific antibodies with quantum dots is used to save experimental time and improve work efficiency. The expression of B cells and Breg cells in the thymus immune microenvironment and the expression of high endothelial venules can be detected, and at the same time, the relative spatial positions of the above cells and blood vessels can be observed, which directly reflects the state of immune infiltration and autoimmune reaction in the thymus immune microenvironment, and has broad application prospects in the thymus-related immunity and tumor fields.

Human herpesviruses can infect barrier and immune cells of the intestinal tract to cause microbiome dysbiosis and inflammation. Microbiome dysbiosis can affect the availability of nutrients required for normal brain function. Inflammation can compromise the intestinal barrier and lead to microbial translocation. Microbial translocation can cause brain infection or a mimicry auto-immune response. The embodiments restrict herpesvirus activity and injury by 1) the oral administration of exosomes containing factors to inhibit viral activity and restore homeostasis, and 2) the oral administration of recombinant bacteria that produce exosomes containing factors to inhibit viral activity and restore homeostasis. Another embodiment is the treatment of alpha-HHVs mediated intestinal dysfunction by nucleoside analogs, such as famciclovir, which may be combined with anti-viral exosome therapy.

To provide a consensus prostate antigen, a nucleic acid molecule encoding the same, a vaccine containing the same and use thereof.SOLUTION: Provided herein are consensus amino acid sequences of prostate antigens capable of breaking tolerance in a target species, including PSA, PSMA, STEAP, and PSCA antigens. Also provided are nucleic acid sequences encoding a consensus amino acid sequence of one or more of the prostate antigens PSA, PSMA, STEAP, and PSCA, as well as genetic constructs / vectors and vaccines expressing such sequences. Also provided herein are methods of generating an autoimmune response against prostate cancer cells by administering one or more of the provided vaccines, proteins, and / or nucleic acid sequences.SELECTED DRAWING: None

The present invention relates to tetrahydrobenzo-isoquinoline sulfonamide derivatives of formula (I), processes for preparing them, pharmaceutical compositions containing them and their use in treating disorders caused by IgE (such as allergic responses, non-allergic mast cell responses or certain autoimmune responses), and in particular disorders caused by the interaction of IgE with the FcεRI receptor.

The invention discloses a humanized monoclonal antibody of a beta1-adrenergic receptor as well as a kit and application of the humanized monoclonal antibody. The amino acid sequence of the humanized monoclonal antibody of the beta1-adrenergic receptor is as shown in SEQ ID No.1. The invention further discloses a preparation method of the humanized monoclonal antibody of the beta1-adrenergic receptor. According to the distribution condition of myocardial antigenic determinants, polypeptides of natural antigenic determinants are designed and synthesized to immunize animals to prepare monoclonal antibodies and carry out humanized expression, so that the antibody detection kit is prepared. The kit can be used for auxiliary diagnosis of autoimmune response activation and prognosis judgment of patients with viral myocarditis and dilated cardiomyopathy, and auxiliary establishment of a patient treatment scheme.

The present invention relates to a composition for preventing or treating Behcet's disease and rheumatoid arthritis, the composition containing a peptide or a mixture thereof as an active ingredient. More specifically, an intraperitoneal injection or application of P1 to P5 peptides or a mixture thereof as a skin external preparation to a mouse animal model having Behcet's disease caused by autoimmune response was found to ameliorate skin ulcers and skin inflammation in the Behcet's disease mouse model, and an arthritis amelioration effect on a rheumatoid arthritis animal model was also observed. Accordingly, the composition containing P1 to P5 peptides or mixtures thereof as active ingredients can be provided as medicine for Behcet's disease and rheumatoid arthritis.

The present invention relates to a peptide for treating inflammation and wounds and, more specifically, to use of a peptide for treating inflammation and wounds, wherein the peptide binds to collagen type VII exposed by damage to tissue and recognizes collagen type VII as an antigen, thereby inhibiting the induction of an immune response, and thus having a function of inhibiting inflammation caused by an autoimmune response, and has the function of promoting wound healing by promoting cell proliferation and migration to a wound site in the damaged tissue. The peptide according to the present invention has the binding ability to collagen type VII, and thus inhibits an immune response caused by collagen type VII, thereby inhibiting inflammation caused by an autoimmune response. In addition, the peptide can bind to the integrin beta 1 of intestinal epithelial cells and increase the cell adhesion and migration via phosphor-FAK signal and tight junction markers are increased via FAK-RhoA signal and thus promote intestine regeneration.

This invention provides combinations of kynurenine and antigen presenting cells (APC) for modulating immune tolerance, wherein the combinations may be used to modulate an autoimmune response, which may be of use in the treatment of Type 1 Diabetes (TID)) or alopecia areata (AA). Uses of kynurenine and antigen presenting cells (APC) as an immune modulator for the treatment of TID or AA are also provided.

This disclosure relates to modulating IL-2 expression / activity to prevent or treat diseases (cancer, autoimmune diseases, inflammatory diseases, or infections). Compounds of formula (I), as well as compositions comprising their conjugates, complexes, and pharmaceutical compositions, as well as methods of using them to modulate (e.g., increase) IL-2 expression / activity to achieve desired results (e.g., reduction in cancer cell viability, growth, proliferation, or metastasis; reduction in tumor volume; increase in survival; increase or decrease in immune cell proliferation or activation; increase or decrease in cytokine production; decrease in autoimmunity; decrease in inflammation, etc.). Related pharmaceuticals, kits, and methods of delivering such compositions are described. Compounds of formula (I) and methods for developing or manufacturing their pharmaceutical compositions are provided. Diagnostic and test methods for detecting levels of IL-2 expression / activity, as well as compositions constituting diagnostic or test kits, are further described. JPEG2026513223000025.jpg3642

The invention discloses a pMHC binding agent and application thereof. The antigen peptide-major histocompatibility complex binding agent comprises four RNA molecules, wherein the first RNA molecule comprises an antigen peptide, a DRB1 * 13: 02 beta chain, a mouse I-Eb binding segment and nucleic acid molecules coded by CD28 and CD3 zeta proteins of transmembrane and intracellular segments; the second RNA molecule comprises CMV, CD74, an antigen peptide and a nucleic acid molecule coded by a red visible spectrum fluorescent protein; the third RNA molecule comprises CD4 and a nucleic acid molecule coded by a T cell surface receptor binding region peptide sequence; and the fourth RNA molecule comprises mCD40L and a nucleic acid molecule coded by a binding peptide fragment for recognizing pMHC. According to the present invention, the antigen peptide-major histocompatibility complex II type molecule and the T cell surface receptor can be efficiently and specifically combined so as to promote the activation of the target cell surface receptor so as to achieve the efficient autoimmune reaction;