28 results about "CD5" patented technology

The invention discloses a kit and method for detecting leukemia and lymphoma based on full-spectrum flow cytometry, the kit comprises 25 antibodies, the antibodies are specifically bound with fluorescein respectively, and leukemia and lymphoma are detected through full-spectrum flow cytometry; the 25 kinds of antibodies comprise HLA-DR (human leukocyte antigen-DR), CD38, CD7, CD34, Lambda, CD19, CD64, CD14, CD5, CD123, CD16, CD20, Kappa, CD117, CD13, CD45, CD11b, CD2, CD10, CD8, CD15, CD4, CD3, CD56 and CD33. The kit comprehensively covers development stages of various lines of bone marrow cells, and common abnormal expressions of various leukemia, myelodysplastic syndromes and lymphoma, and can preliminarily screen various leukemia and lymphoma.

The invention relates to an antibody composition for detecting abnormal CTL (cytotoxic T lymphocyte) cells of hemophagocytic syndrome and application of the antibody composition, and the antibody composition comprises a CD2 antibody, a CD3 antibody, a CD4 antibody, a CD5 antibody, a CD7 antibody, a CD8 antibody, a CD56 antibody, a CD57 antibody, a Granzyme B antibody, a Perforin antibody, a TRBC1 antibody and a CD45 antibody. In the technical scheme provided by the invention, key phenotypic characteristics of CTL (Cytotoxic Lymphocyte) can be completely covered by various antibodies aiming at T cell and NK cell surface markers, T large granular lymphocyte markers, cytotoxic granular proteins, T cell receptor constant regions and leukocyte common antigens; wherein the clonality of the CTL cells is judged through the expression level of the TRBC1 antibody, and the cytotoxic function activity of the CTL cells is evaluated through the expression levels of Granzyme B and Perforin.

The application belongs to the technical field of biological medicine, and discloses a cyclic peptide molecule specifically targeting CD5 and purposes thereof. The surface receptor CD5 of immune cells (T cells, B cells) has been proved to be a potential tumor treatment target, the present application uses the phage display technology widely applied to the development of polypeptide or antibody drugs to carry out multiple rounds of in vitro screening on human CD5 protein, and obtains a cyclic peptide molecule with drug potential and capable of specifically combining with CD5 through second-generation sequencing. The cyclic peptide molecule contains two cysteines, is modified into a ring through a specific chemical crosslinking agent, and the affinity of the cyclic peptide molecule to CD5 is determined to be in the low micromolar level through surface plasmon resonance technology, thereby laying a foundation for the development of a CD5-targeting inhibitor.

The present invention provides a pluripotent stem cell into which a nucleic acid encoding a chimeric antigen receptor (CAR) specific to CD5, CD2, or CD6 has been introduced. The present invention also provides a CAR-T cell specific to CD5, CD2, or CD6, which is obtained by inducing the differentiation of the pluripotent stem cell into a T cell, and has the following characteristics: (a) that the expression of CD5, CD2, and CD6 is reduced compared to that of a corresponding CAR-T cell derived from peripheral blood; and (b) that cytotoxic activity against T-cell tumors is higher than that of the corresponding CAR-T cell and a CD5, CD2, or CD6 gene-deficient CAR-T cell, which are derived from peripheral blood.

This embodiment provides cells containing heterologous nucleic acid molecules inserted at the CD5 gene locus. A composition containing such cells, as well as methods for producing and using such cells and compositions, are also provided herein.

The invention relates to the technical field of biological medicine, in particular to application of S100A9 protein to preparation of a product for predicting the recurrence risk of AML. The product is used for detecting a marker CD15, a marker CD33, a marker CD14, a marker CD15, a marker CD33, a marker CD64, a marker CD5, a marker CD14, a marker CD10, a marker CD19, a marker CD33, a marker CD34, a marker CD64, a marker CD117, a marker CD13 or a marker CD45. Therefore, the accuracy of predicting the AML recurrence risk is improved.

The invention discloses a method for detecting non-target cells in amniotic epithelial cells, which comprises reagents for detecting one or more of the following gene markers: FCGBP, RNASE6, DAB2, STAB1, RAB3IL1, CSF1R, CD68, CD209, EGFL7, LGALS2, LILRB4, HLA-DMB, HLADMA, CD74, ANPEP, CD44, CCR7, CD3G, CD3D, CD27, CD5, SPOCK2, TCF7, GZMH, KLRC2 and the like. Wherein the non-target cells are selected from macrophage-like cells, monocyte-like cells, T cell-like cells, NK cell-like cells, myeloid-like cells and neutrophil-like cells, a detection method is provided for quality control of the amniotic epithelial cells, and guidance is also provided for a cell product preparation process.

The present disclosure features polypeptides capable of binding to Cluster of Differentiation 5 (CD5) antigens and polynucleotides encoding the CD5 binding polypeptides, compositions comprising them, and methods of use thereof. The disclosure also features lipid nanoparticles comprising the CD5 binding polypeptides and methods of use thereof for delivering polynucleotides (e.g., polynucleotides encoding chimeric antigen receptors) to T cells in vivo.

The present disclosure provides delivery particles comprising: (a) a targeting moiety on the surface of the particle, wherein the targeting moiety comprises an antibody or an antigen-binding fragment thereof that binds to a T cell antigen selected from CD5, CD7, and CD27; and (b) a payload encapsidated within the particle. The disclosure provides methods of using the particles.

The invention relates to application of a CD2 / 5 / 7 knockout anti-CD2 / 5 / 7 chimeric antigen receptor T cell to T cell lymphoma and leukemia. The present invention includes compositions and methods for treating T cell lymphoma and leukemia. In certain aspects, the compositions and methods include CAR T cells that target CD2, CD5, or CD7 and modified cells in which CD2, CD5, or CD7 has been knocked out.

The application discloses a simple and low-cost method for culturing canine NK cells in vitro and belongs to the technical field of cell culture. The method comprises the following steps: separating NK cells from peripheral blood of a dog, culturing the NK cells with a canine NK cell activation culture medium for 24-48 hours, then continuing to culture the NK cells with a canine NK cell expansion culture medium, adding the canine NK cell expansion culture medium after 48 hours, expanding the cells in a bottle when the cells are obviously expanded, otherwise maintaining the cells in the original bottle after centrifugation, adding liquid and expanding the cells in a bottle or culturing the cells in the original bottle every other day, and harvesting the canine NK cells after 12-18 days. The method provided by the application does not need to activate the canine NK cells by using engineered trophoblast cells and multiple cell factors, and does not need to activate the cells by using an antibody, so that the method is simple and low in cost, and the cultured canine NK cells normally express NKp46, do not express CD3 and CD5, and have normal inhibitory and killing tumor abilities.

The invention provides application of a CD5-targeting reagent in the aspects of reducing the drug resistance of tumor cells and improving the anti-tumor curative effect of drugs, and clarifies for the first time that CD5 molecules can promote high expression and cell nucleus displacement of transcription factors FOXO3a and FOXO4 in a forkhead cassette O signal channel; therefore, expression increase of the ABC drug-resistant protein family in diffuse large B-cell lymphoma tumor cells is mediated, and drug resistance of tumor cells to various chemotherapeutic drugs is promoted. Further, it is found that the celecoxib can significantly inhibit expression of CD5 molecule mediated ABC drug-resistant protein in B-cell lymphoma cells, then the celecoxib and chemotherapeutic drugs are combined for application, the killing effect of traditional chemotherapeutic drugs on diffuse large B-cell lymphoma tumor cells is significantly enhanced, and the chemotherapeutic drug resistance of diffuse large B-cell lymphoma is overcome. The anti-drug-resistant tumor strategy can overcome the problems of low treatment response rate and poor prognosis of the CD5-positive diffuse large B-cell lymphoma to the existing chemotherapy regimen due to multidrug resistance, and significantly improves the anti-tumor treatment effect.

This invention discloses an anti-CD5 protein nanobody and its applications, relating to the field of nanobody biosynthesis technology. Utilizing a camel-derived nanobody library and targeting mouse CD5 protein, this invention employs phage display technology for in vitro enrichment and panning. Camel-derived nanobody sequences targeting CD5 protein are obtained through monoclonal high-throughput ELISA screening. These five nanobody sequences can be used to detect CD5 protein expression, for the diagnosis and screening of related tumors, and also for the preparation of drugs to treat related tumors.

This invention provides a method for screening peptides that specifically target T cells, comprising providing T cells having a subset selected from CD1, CD2, CD3, CD4, CD5, CD7, CD8, CD16, CD25, CD26, CD27, CD28, CD30, CD38, CD39, CD40L, CD44, CD45, CD62L, CD69, CD73, CD80, CD83, CD86, CD95, CD103, CD119, CD126, CD150, CD152 (CTLA-4), CD153, CD154 (CD40L) The T cells are labeled with at least one of the following surface antigen markers: CD161, CD183, CD223, CD254, CD275, CD45RA, CXCR3, CXCR5, FasL, IL18R1, CTLA-4, OX40, GITR, LAG3, ICOS, PD-1, leu-12, TCR, TLR1, TLR2, TLR3, TLR4, TLR6, NKG2D, CCR, CCR1, CCR2, CCR4, CCR6, and CCR7. The T cells are then contacted with a peptide display library, and target peptides that specifically bind to the T cells are screened therefrom.

The invention discloses a simple and low-cost method for culturing canine NK cells in vitro, and belongs to the technical field of cell culture. The method comprises the following steps: separating NK cells from peripheral blood of a dog, culturing for 24-48 hours by using a dog NK cell activation culture medium, then continuously culturing by using a dog NK cell amplification culture medium, supplementing the dog NK cell amplification culture medium after 48 hours, expanding a bottle if the cells are obviously amplified, otherwise, maintaining original bottle culture after centrifuging, and subsequently supplementing liquid and expanding the bottle or performing original bottle culture every two days, and harvesting the canine NK cells after 12-18 days. According to the method provided by the invention, engineering trophoblasts and multicellular factors are not needed to activate the canine NK cells in the whole process, antibody coating activation is also not needed, the operation is simple and convenient, the cost is relatively low, and the cultured canine NK cells normally express NKp46, do not express CD3 and CD5 and have normal tumor inhibiting and killing capabilities.

This invention belongs to the field of biodetection technology, specifically relating to early warning biomarkers for Sjögren's syndrome and their applications. The biomarkers include plasma proteins selected from LGALS9, TNFRSF9, and CD5 proteins. The AUC value of this biomarker for early prediction of Sjögren's syndrome is 0.69.

Provided is a method for screening polypeptides that specifically target T cells, comprising: providing T cells having a surface antigen marker selected from at least one of CD1, CD2, CD3, CD4, CD5, CD7, CD8, CD16, CD25, CD26, CD27, CD28, CD30, CD38, CD39, CD40L, CD44, CD45, CD62L, CD69, CD73, CD80, CD83, CD86, CD95, CD103, CD119, CD126, CD150, CD152 (CTLA-4), CD153, CD154 (CD40L), CD161, CD183, CD223, CD254, CD275, CD45RA, CXCR3, CXCR5, FasL, IL18R1, CTLA-4, OX40, GITR, LAG3, ICOS, PD-1, leu-12, TCR, TLR1, TLR2, TLR3, TLR4, TLR6, NKG2D, CCR, CCR1, CCR2, CCR4, CCR6, and CCR7; and contacting the T cells with a polypeptide display library, and screening therefrom target polypeptides that specifically bind to the T cells.

The application discloses a VSIG4 antibody and application thereof, and relates to the technical field of biological medicines. The antibody provided by the application can block VSIG4-CD5 interaction, thereby relieving tumor progression.

The present invention relates to a novel anti-CD5 chimeric antigen receptor and use thereof. The chimeric antigen receptor of the present invention can specifically bind to the extracellular membrane-proximal domain of CD5, and immune cells expressing the chimeric antigen receptor exhibit reduced reactivity with respect to normal cells expressing CD5, and thus the present invention can be used as an efficient therapeutic agent for various CD5-mediated cancer diseases.

The present invention provides compositions and methods for treating T-cell lymphoma and T-cell leukemia. [Solution] A method for treating cancer comprising the steps of administering a first modified cell containing a chimeric antigen receptor (CAR) comprising an antigen-binding domain, a transmembrane domain, and an intracellular domain to the subject, and administering a second modified cell in which the endogenous CD5 gene is knocked out to the subject. Preferably, the antigen-binding domain is an antigen-binding domain that can bind to CD2, CD5, or CD7, and preferably the endogenous CD5 gene is knocked out by the CRISPER / Cas9 method.

The present invention is directed to the field of immunotherapy, in particular, adoptive T cell therapy or T cell receptor (TCR) gene therapy of cancer. The invention provides nucleic acids encoding at least one TCR alpha or beta chain construct of a TCR construct capable of specifically binding to a peptide from the T-cell lineage specific antigen CD5, preferably SEQ ID NO: 1 or 33, in the context of a human MHC I such as HLA-A*02, in particular HLA-A*02:01. The invention also provides corresponding proteins and host cells, preferably, CD8+ T cells, expressing said TCR construct. Treatment optionally is in the context of allogeneic stem cell transplantation, in particular, mismatch-transplantation, or haploidentical transplantation, or in combination with an agent capable of inhibiting expression of HLA-A*02 in the TCR-transgenic T cells. The invention thus also provides compositions and kits comprising the nucleic acids of the invention in combination with an agent capable of inhibiting expression of HLA-A*02, and, as well as the medical use of such compositions and kits. The nucleic acids, compositions and kits, proteins or host cells may be for use in the diagnosis, prevention and / or treatment of a CD5-positive T-cell lymphoma or T-cell leukemia, no matter whether the antigen is expressed on the cell surface, intracytoplasmic or in both manners.

Provided herein are, inter alia, antibodies (e.g., humanized antibodies, monoclonal antibodies) and antibody compositions (e.g., chimeric antigen receptors, bispecific antibodies) that are capable of binding CD5. The antibodies and antibody compositions provided herein include novel light and heavy chain domain CDRs and framework regions, and bind CD5 with high efficiency and specificity, thereby effectively targeting CD5 expressing cells. The antibodies provided herein may form part of recombinant proteins also referred to herein as antibody compositions (e.g., chimeric antigen receptors or bispecific antibodies) to be used, inter alia, for therapeutic cancer applications.

A preparation method for and a use of a chimeric antigen receptor (CAR)-γδT cell for immunotherapy of T cell acute lymphoblastic leukemia, relating to the field of biomedicine. The provided anti-CD5 nanobody can specifically bind to a CD5 antigen, and has good affinity. By using the anti-CD5 nanobody as an antigen-binding domain to construct a CAR, the prepared CAR-γδT cell exhibits significant killing activity against CD5-positive tumor cell lines, such as T cell acute lymphoblastic leukemia cells.

The invention provides a preparation method and application of an in-vivo CAR-T cell for treating interstitial lung disease, and provides a T cell of a chimeric antigen receptor which is modified by genetic engineering and is used for expressing targeted fibroblast activating protein. A targeted fibroblast activation protein (FAP) CAR-T cell therapy model is constructed by targeting CD5 entrapped mRNA nano-liposome (LNP) transfection and lentiviral vector, and the method comprises the following steps: firstly, verifying the difference of the killing ability of FAP CAR-T constructed by CD5 LNP-mRNA and lentivirus in a 293T cell which stably co-expresses FAP, Luciferase and mCherry, and then verifying the difference of the killing ability of FAP CAR-T constructed by LNP-mRNA and lentivirus in the 293T cell which stably co-expresses FAP, Luciferase and mCherry; further verifying the effectiveness of the CAR-T cells constructed by transfecting the CD5 LNP-mRNA on cell lines of human fibroblasts (CDD19Lu, LL29 and LL97A) and primary fibroblasts of human and mice in vitro, and further verifying the effectiveness and safety of the CD5 LNP-FAP CAR-T in treatment of pulmonary fibrosis through in-vivo experiments in animals. A novel and effective anti-fibrosis treatment thought is provided for patients with fibrosis interstitial lung diseases.

The present invention relates to immune cells co-expressing a chimeric antigen receptor comprising an OX40 ligand as an intracellular signaling domain and IL-15, and a composition for preventing or treating cancer comprising the same as an active ingredient. The immune cells of the present invention not only exhibit synergistic tumor cell-killing activity by co-expression of the chimeric antigen receptor and IL-15, but also have significantly improved viability and in vitro proliferation rate, and thus they may be used as an efficient anticancer cell therapy. In particular, the immune cells of the present invention, when expressing a chimeric antigen receptor targeting CD5, may be applied as an effective therapeutic composition for various CD5-positive tumors, including lymphocytic leukemia.

The present invention relates to a novel antibody against CD5 and uses thereof. The antibody of the present invention exhibits high binding affinity to and inhibitory activity against CD5 protein, and thus can be utilized as an effective therapeutic agent for various CD5-mediated cancer diseases.

There is provided a method of identifying pro-inflammatory dendritic cells, the method comprising: determining an expression of CD5, CD14 and / or CD163 in cells, wherein CD5−, CD14+ and / or GD163+ cells are identified as pro-inflammatory dendritic cells. Also disclosed is a method of characterising inflammation and / or inflammatory disease in a subject, the method comprising: determining a proportion of CD5−, CD14+ and / or GD163+ dendritic cells in the subject's sample, wherein the proportion positively correlates with the level of inflammation and / or the severity of inflammatory disease in the subject.