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背景介绍 ICOSL is the Ligand for the T-cell-specific cell surface receptor ICOS. When engaged by the ICOSL, the ICOS initiates a costimulatory signal for T-cell proliferation and cytokine production. It also induces B-cell proliferation and differentiation into plasma cells. The ICOS/ICOSL is a major regulator of the adaptive immune responses and also plays an important role in mediating local tissue responses to inflammatory conditions. 产品介绍 Recombinant CHO-K1 cells constitutively expressing human ICOSL (also known as human secreted B7 homolog 2 (B7-H2), CD275, ICOSLG, and B7-related protein (B7RP), GenBank Accession No. NM_001283050.
询价背景介绍 The binding of Programmed Cell Death Protein 1 (PD-1), a receptor expressed on activated T-cells, to its ligands, PD-L1 and PD-L2, negatively regulates immune responses. PD-1 ligands are found on most cancers, and the PD-1:PD-L1/2 interaction inhibits T-cell activity and allows cancer cells to escape immune surveillance. The PD-1:PD-L1/2 pathway is also involved in regulating autoimmune responses, making these proteins promising therapeutic targets for a number of cancers, as well as multiple sclerosis, arthritis, lupus, and type I diabetes. 产品介绍 Recombinant CHO-K1 cells constitutively expressing human PD-L2 (Programmed Cell Death 1 Ligand 2 or CD273, GenBank accession #NM_025239) and an engineered T-cell receptor (TCR) activator.
询价背景介绍 CD160 is a glycosylphosphatidylinositol (GPI)-anchored protein member of the Ig superfamily that is expressed at the cell surface and highly restricted to circulating NK and T cells. Binding of CD160 to both classical and non-classical MHC I enhances NK and CD8+ CTL functions. However, engagement of CD160 by the Herpes Virus Entry Mediator (HVEM / TNFRSF14) was shown to mediate inhibition of CD4+ T-cell proliferation and TCR-mediated signaling. HVEM protein is a bimolecular switch that binds both co-stimulatory LT-α/LIGHT and co-inhibitory receptors CD160/BTLA. The binding of coinhibitory receptors CD160 and/or BTLA on T cells with HVEM expressed on DC or Tregs transduces negative signals into T cells that are counterbalanced by costimulatory signals delivered after direct engagement of HVEM on T cells by LIGHT expressed on DC or more likely, on other activated T cells (T-T cell cooperation). HVEM was also shown to be expressed in the majority of cultured melanoma cell lines and metastatic melanoma samples. The predominance of the interaction of HVEM with CD160 and BTLA over the HVEM/LIGHT pathway or vice versa might be the result of differences in ligand/receptor affinity and the differential expression pattern of these molecules on cell types at different stages of cell differentiation. LIGHT, BTLA, and CD160 have substantially different binding affinities and occupy spatially distinct sites upon interaction with the HVEM receptor, which enables HVEM to function as a molecular switch. The net effect of the LIGHT/HVEM and HVEM/BTLA/CD160 interaction, when these different receptors and ligands are simultaneously present, determines the outcome of the response. CD160/HVEM interaction plays a key role in the regulation of inflammatory, autoimmune, and antitumor responses, and is an important target for cancer immunotherapy drug discovery. The interaction of CD160 on tumor specific T cells and HVEM on melanoma cells resulted in T cell inhibition, which could be reversed by treatment with anti-CD160 blocking antibody. Therapeutically targeting CD160 and HVEM remains a focus for in pre-clinical studies as the bidirectional signaling pathways of CD160/BTLA/HVEM and HVEM/LIGHT are further elucidated. 产品介绍 Recombinant Jurkat T cell expressing firefly luciferase gene under the control of NFAT response elements with constitutive expression of human CD160. CD160 is a GPIanchored glycoprotein member of the Ig superfamily, also known as BY55, NK1, and NK28. GenBank Accession # NM_007053.
询价背景介绍 HVEM is a member of the TNFR superfamily that is expressed on T cells, B cells, NK cells and antigen-presenting cells. HVEM is a bidirectional switch that regulates T-cell activation in either a costimulatory or coinhibitory fashion, depending on the binding partner. HVEM can act as both ligand and receptor; the binding of HVEM to BTLA (IgSF) or CD160 on Effector T cells delivers a coinhibitory signal; alternately, the binding of HVEM to either of two tumor necrosis factor ligands, LIGHT or lymphotoxin-α, delivers a costimulatory signal. The HVEM/BTLA axis are co-inhibitory immune checkpoint molecules that play important roles in the blockade of T cell-mediated immune responses. The binding of BTLA, a receptor expressed on activated T-cells, to its ligand HVEM, found on melanoma and other cancers, negatively regulates T cell immune responses and allows cancer cells to escape immune surveillance. This co-inhibitory signal of the HVEM/BTLA interaction can be reversed by treatment with a BTLA blocking antibody. The HVEM/BTLA/LIGHT pathway is also involved in regulating autoimmune responses, making these proteins promising therapeutic targets for a number of diseases. 产品介绍 Recombinant CHO-K1 cells constitutively expressing human HVEM (Herpes Virus Entry Mediator), also known as CD270 or TNFRSF14 (Tumor Necrosis Factor Receptor Superfamily Member 14), GenBank Accession No. NM_003820, and an engineered T cell receptor (TCR) activator.
询价背景介绍 CTLA4, also known as CD152, is a protein receptor that functioning as an immune checkpoint. It is expressed by activated T cells and transmits an inhibitory signal to T cells. CTLA4 is homologous to the T-cell co-stimulatory protein, CD28, and both molecules bind to CD80 (B7-1) and CD86 (B7-2) on antigen-presenting cells. CTLA-4 binds to CD80 and CD86 with greater affinity and avidity than CD28 thus enabling it to outcompete CD28 for its ligands and act as an "off" switch when bound to CD80 or CD86. CTLA-4 is an important immunotherapy target for the treatment of cancer and autoimmune diseases. 产品介绍 Recombinant Jurkat T cell expressing firefly luciferase gene under the control of IL-2 promoter with constitutive expression of human CTLA4 (Cytotoxic T-Lymphocyte Associated Protein, CD152; GenBank Accession #NM_005214).
询价背景介绍 Fc Gamma Receptor 2B (FcGR2B, FcγRIIB), also known as CD32B, is a "low affinity" receptor for Immunoglobulin G (IgG). FcGR2B is involved in the phagocytosis of immune complexes and in the regulation of antibody production by B-cells. Mutations in the gene encoding FcGR2B have been linked to systemic lupus erythematosus (SLE). FcGR2B is the predominant Fc receptor present on B cells, and high expression of FcγRIIB negatively regulates mAb-mediated immunotherapy. Therefore, FcGR2B is an important immunotherapy target, both directly for B-cell malignancies and in combination with clinically relevant therapeutic mAbs to overcome FcGR2B-mediated resistance. 产品介绍 Recombinant FcGR2B-CHO K1 cell line stably expressing full length human FcGR2B (isoform 1, GenBank Accession Number NM_004001.4). Crosslinking of antibodies bound to target by FcGR-expression cells can promote receptor clustering and increase downstream signaling. FcGR2B crosslinking is important for anti-TNFR receptor antibodies.
询价背景介绍 CD70, also known as TNFSF7, is a cytokine which binds to CD27. CD70 is involved in T-cell activation and induces the proliferation of costimulated T-cells. Moreover, TNFSF7 enhances the generation of cytolytic T-cells. This cytokine is also reported to play a role in regulating B-cell activation, cytotoxic function of natural killer cells, and immunoglobulin synthesis. Diseases associated with CD70 include acute myocarditis, arthritis, and other inflammatory disorders. 产品介绍 Recombinant CHO-K1 cells constitutively expressing human CD70 (also known as Tumor Necrosis Factor Ligand Superfamily Member 7, TNFSF7, CD27 Ligand, Ki-24 antigen, CD27-L, and CD27LG; GenBank accession #NM_001252).
询价背景介绍 CD27 is a member of the tumor necrosis factor (TNF) receptor superfamily, which includes the T cell co-stimulatory receptors OX40, 4-1BB and herpesvirus entry mediator (HVEM). CD27 is expressed on various types of T cells, B cells and a subset of natural killer cells. It activates NF-κB and MAPK/JNK signaling upon interaction with its TNF-like ligand, CD70, which is expressed by numerous tumor cells. Adaptor proteins TRAF2 and TRAF5 can also stimulate CD27 signaling. Activation of CD27 leads to lymphoid proliferation, differentiation, apoptosis, and the induction of long-term memory. The CD27/CD70 pathway is a key target for the development of treatments for cancer and inflammatory diseases. 产品介绍 Recombinant Jurkat T cell expressing firefly luciferase gene under the control of NF-kB response elements with constitutive expression of human CD27 (also known as Tumor Necrosis Factor Receptor Superfamily Member 7, TNFRSF7, and T14, Genbank Accession #BC012160)
询价背景介绍 BTLA is an immunoglobulin domain-containing glycoprotein expressed on T cells, resting B cells, macrophages, DCs and, to a lesser extent, NK cells. BTLA acts as an inhibitory receptor on T cells, as anti-BTLA treatment results in T cell proliferation, and BTLA knockout mice demonstrate hyper-responsive immune activation. Subsequently, herpesvirus entry mediator (HVEM), a tumor necrosis factor receptor, was identified as a natural ligand for BTLA in mice and humans. Expression of HVEM by antigen-presenting cells (APCs) was capable of inducing BTLA-dependent T cell inhibition. BTLA belongs to the immunoglobulin superfamily, along with CTLA-4 and PD-1, which characteristically binds to B7 family members. HVEM is a member of the tumor necrosis factor receptor family, and the BTLA/HVEM interaction is the first to demonstrate crosstalk between these two receptor families. Prior to the discovery of the BTLA/HVEM interaction, HVEM was known to bind LIGHT and lymphotoxin-α, both tumor necrosis factor ligands. While the BTLA/HVEM interaction results in a co-inhibitory signal, the HVEM/LIGHT interaction results in a co-stimulatory signal through HVEM. In melanoma patients, BTLA was demonstrated to be expressed on tumor-specific T cells both in circulation and in metastatic lymph nodes. HVEM was subsequently shown to be expressed in the majority of cultured melanoma cell lines and metastatic melanoma samples. The interaction of BTLA on tumor specific T cells and HVEM on melanoma cells resulted in T cell inhibition, which could be reversed by treatment with a BTLA blocking antibody. BTLA/HVEM interaction plays a key role in the regulation of inflammatory, autoimmune, and antitumor responses, and is an important target for cancer immunotherapy drug discovery. Therapeutically targeting BTLA and HVEM remains in pre-clinical stages as the bidirectional signaling pathways of BTLA/HVEM and HVEM/LIGHT are further elucidated. 产品介绍 Recombinant Jurkat T cell expressing firefly luciferase gene under the control of NFAT response elements with constitutive expression of human BTLA (B and T lymphocyte associated, B and T lymphocyte attenuator, BTLA1, CD272, GenBank Accession #NM_181780).
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