IL-10 Monoclonal Antibody (JES3-9D7)
货号:14-7108-81,14-7108-85
规格:50μg,500μg
价格:1130,3249
产品类型:抗体和染料
品牌:eBioscience
物种:人
宿主:大鼠
抗体亚型:IgG
克隆号:JES3-9D7
荧光染料:其它
类型: | 单抗 | 同型对照: | |
浓度: | 0.5 mg/mL | 用法: | 1-4 µg/mL (ELISA);Assay-Dependent (IHC (P)) |
产品详细信息Description: The JES3-9D7 monoclonal antibody reacts with human interleukin-10 (IL-10).Applications Reported: The JES3-9D7 antibody has been reported for use in capture of human IL-10 by ELISA, intracellular flow cytometric analysis, and for neutralizing IL-10 bioactivity. (Use Functional Grade purified for functional studies cat. 16-7108).Applications Tested: The JES3-9D7 antibody has been tested as the capture antibody in a sandwich ELISA for analysis of human Interleukin-10 (IL-10) in combination with the biotin JES3-12G8 (13-7109) antibody for detection and recombinant human IL-10 (14-8109) as the standard. A suitable range of concentrations of this antibody for ELISA capture is 1-4 µg/mL. A standard curve consisting of doubling dilutions of the recombinant standard over the range of 1000 pg/mL - 8 pg/mL should be included in each ELISA plate.Purity: Greater than 90%, as determined by SDS-PAGE.Aggregation: Less than 10%, as determined by HPLC.Filtration: 0.2 µm post-manufacturing filtered.靶标信息Interleukin 10 (IL-10, CSIF) is an anti-inflammatory cytokine mainly produced by macrophages and Th2 cells. IL-10 is an 18.6 kDa protein of 160 amino acid residues that shares over 80% sequence homology with the Epstein-Barr Virus protein (BCRFI). The reported biological activities of IL-10, which maybe interrelated, include inhibition of macrophage-mediated cytokine synthesis, suppression of the delayed-type hyper-sensitivity response, and stimulation of the Th2 cell response which results in elevated antibody production. IL-10 functions by inhibiting pro-inflammatory cytokines made by macrophages and regulatory T cells including IFN-gamma, TNF-alpha, IL-2, and IL-3, IL-4, and GM-CSF. IL-10 is also known to suppress antigen presentation on antigen presenting cells, enhances B cell survival, proliferation, and antibody production. IL-10 can block NF-kappa B activity, and is involved in the regulation of the JAK-STAT signaling pathway. While human IL-10 can act on murine cells, murine IL-10 cannot act on human cells. Binds to a retinoid X receptor (RXR) responsive element from the cellular retinol-binding protein II promoter (CRBPII-RXRE). IL-10 inhibits the 9-cis-retinoic acid-dependent RXR alpha transcription activation of the retinoic acid responsive element. Knockout studies in mice suggest the function of this cytokine as an essential immunoregulator in the intestinal tract.
数据 |
IL-10 Antibody (14-7108-81)mSystems 2019 -FIG 2 Spore-forming bacteria from MS patients inhibit IL-10 + Treg differentiation in vitro . (A and B) Representative flow cytometry plots (A) and quantification (B) of CD4 + FoxP3 + Tregs within CD3 + lymphocytes differentiated in response to spore-forming bacteria isolated from controls or untreated MS patients. n = 7 PBMC donors; each dot represents an average response from PBMC donor to isolates from 6 control or MS bacterial donors. * * , P < 0.01, two-tailed repeated measures t test. (C and D) Representative flow cytometry plots (C) and quantification (D) of IL-10 + lymphocyte population within CD3 + CD4 + FoxP3 + Tregs differentiated in response to spore-forming bacteria isolated from controls or untreated MS patients. n = 6 bacterial donors per group. * , P < 0.05, two-tailed t test. Error bars, mean +- SEM. The experiment was repeated with nonoverlapping PBMC and bacterial donors and gave the same results. (E) Quantification of T effector cell proliferation in response to Tregs differentiated in the presence of spore-forming bacteria from MS patients or controls. n = 3 bacterial donors per group, each representing an average of 3 technical replicates. (F) Linear correlation between IL-10 + population within CD3 + CD4 + FoxP3 + Tregs and Clostridia-Bacilli relative abundances. R 2 = 0.214, P = 0.0459. Black dots, MS patients. Light gray dots, controls. |
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