EasySep™小鼠CD90.2正选试剂盒II

免疫磁珠正选细胞分选试剂盒

产品号 #(选择产品)

产品号 #18951_C

免疫磁珠正选细胞分选试剂盒

产品优势

  • 快速、易于操作
  • 纯度高达98%
  • 无需分离柱
  • 分选得到的细胞无荧光标记

产品组分包括

  • EasySep™小鼠CD90.2正选试剂盒II(产品号 #18951)
    • EasySep™小鼠CD90.2正选试剂盒II组分A,0.5mL
    • EasySep™小鼠CD90.2正选试剂盒II组分B,0.5mL
    • EasySep™ Dextran RapidSpheres™ 50100 磁珠,1mL
    • RoboSep™空管
  • EasySep™小鼠CD19正选试剂盒II(产品号 #18951RF)
    • EasySep™小鼠CD90.2正选试剂盒II组分A,0.5mL
    • EasySep™小鼠CD90.2正选试剂盒II组分B,0.5mL
    • EasySep™ Dextran RapidSpheres™ 50100 磁珠,1mL
    • RoboSep™空管
    • RoboSep™ 缓冲液(产品号 #20104)
    • RoboSep™过滤吸头(产品号#20125)x 2
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总览

EasySep™小鼠CD90.2正选试剂盒II专为从脾细胞或其他组织的单细胞悬液中通过正选分离CD90.2+(Thy1.2+)细胞而设计。目的细胞被识别CD14的四聚体抗体复合物和磁珠标记。通过EasySep™磁分选系统 分离被标记目的细胞,无需使用分离柱。目的细胞被保留在分离管中,而非目的细胞倒出即可。 本产品可替代EasySep™小鼠CD90.2阳性分选试剂盒(产品 号#18751),可实现更快速的细胞分选,且分选后的细胞不被PE标记。

磁体兼容性
• EasySep™ Magnet (Catalog #18000) • “The Big Easy” EasySep™ Magnet (Catalog #18001) • EasyEights™ EasySep™ Magnet (Catalog #18103) • RoboSep™-S (Catalog #21000)
 
亚型
细胞分选试剂盒
 
细胞类型
T 细胞
 
种属
小鼠
 
样本来源
其它细胞系,Spleen
 
筛选方法
Positive
 
应用
细胞分选
 
品牌
EasySep,RoboSep
 
研究领域
免疫
 

Data Figures

Typical EasySep™ CD902 Positive Selection Profile

Figure 1. Typical EasySep™ CD90.2 Positive Selection II Profile

Starting with mouse splenocytes, the CD90.2+ cell content of the isolated fraction is typically 95.8 ± 1.5% (mean ± SD using the purple EasySep™ Magnet).

Protocols and Documentation

Find supporting information and directions for use in the Product Information Sheet or explore additional protocols below.

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Applications

This product is designed for use in the following research area(s) as part of the highlighted workflow stage(s). Explore these workflows to learn more about the other products we offer to support each research area.

Resources and Publications

Educational Materials (9)

Publications (2)

Mannan-Binding Lectin Promotes Murine Graft-versus-Host Disease by Amplifying Lipopolysaccharide-Initiated Inflammation. D. Heja et al. Transplantation and cellular therapy 2022 aug

Abstract

Conditioning regimens used for hematopoietic stem cell transplantation (HCT) can escalate the severity of acute T cell-mediated graft-versus-host disease (GVHD) by disrupting gastrointestinal integrity and initiating lipopolysaccharide (LPS)-dependent innate immune cell activation. Activation of the complement cascade has been associated with murine GVHD, and previous work has shown that alternative pathway complement activation can amplify T cell immunity. Whether and how mannan-binding lectin (MBL), a component of the complement system that binds mannose as well as oligosaccharide components of LPS and lipoteichoic acid, affects GVHD is unknown. In this study, we tested the hypothesis that MBL modulates murine GVHD and examined the mechanisms by which it does so. We adoptively transferred C3.SW bone marrow (BM) cells ± T cells into irradiated wild type (WT) or MBL-deficient C57Bl/6 (B6) recipients with or without inhibiting MBL-initiated complement activation using C1-esterase inhibitor (C1-INH). We analyzed the clinical severity of disease expression and analyzed intestinal gene and cell infiltration. In vitro studies assessed MBL expression on antigen-presenting cells (APCs) and compared LPS-induced responses of WT and MBL-deficient APCs. MBL-deficient recipients of donor BM ± T cells exhibited significantly less weight loss over the first 2 weeks post-transplantation weeks compared with B6 controls (P < .05), with similar donor engraftment in the 2 groups. In recipients of C3.SW BM + T cells, the clinical expression of GVHD was less severe (P < .05) and overall survival was better (P < .05) in MBL-deficient mice compared with WT mice. On day-7 post-transplantation, analyses showed that the MBL-deficient recipients exhibited less intestinal IL1b, IL17, and IL12 p40 gene expression (P < .05 for each) and fewer infiltrating intestinal CD11c+, CD11b+, and F4/80+ cells and TCR$\beta$+, CD4+, CD4+IL17+, and CD8+ T cells (P < .05 for each). Ovalbumin or allogeneic cell immunizations induced equivalent T cell responses in MBL-deficient and WT mice, demonstrating that MBL-deficiency does not directly impact T cell immunity in the absence of irradiation conditioning. Administration of C1-INH did not alter the clinical expression of GVHD in preconditioned WT B6 recipients, suggesting that MBL amplifies clinical expression of GVHD via a complement-independent mechanism. WT, but not MBL-deficient, APCs express MBL on their surfaces. LPS-stimulated APCs from MBL-deficient mice produced less proinflammatory cytokines (P < .05) and induced weaker alloreactive T cell responses (P < .05) compared with WT APCs. Together, our data show that MBL modulates murine GVHD, likely by amplifying complement-independent, LPS-initiated gastrointestinal inflammation. The results suggest that devising strategies to block LPS/MBL ligation on APCs has the potential to reduce the clinical expression of GVHD.
Macrophage Coordination of the Interferon Lambda Immune Response. S. A. Read et al. Frontiers in immunology 2019

Abstract

Lambda interferons (IFN-$\lambda$s) are a major component of the innate immune defense to viruses, bacteria, and fungi. In human liver, IFN-$\lambda$ not only drives antiviral responses, but also promotes inflammation and fibrosis in viral and non-viral diseases. Here we demonstrate that macrophages are primary responders to IFN-$\lambda$, uniquely positioned to bridge the gap between IFN-$\lambda$ producing cells and lymphocyte populations that are not intrinsically responsive to IFN-$\lambda$. While CD14+ monocytes do not express the IFN-$\lambda$ receptor, IFNLR1, sensitivity is quickly gained upon differentiation to macrophages in vitro. IFN-$\lambda$ stimulates macrophage cytotoxicity and phagocytosis as well as the secretion of pro-inflammatory cytokines and interferon stimulated genes that mediate immune cell chemotaxis and effector functions. In particular, IFN-$\lambda$ induced CCR5 and CXCR3 chemokines, stimulating T and NK cell migration, as well as subsequent NK cell cytotoxicity. Using immunofluorescence and cell sorting techniques, we confirmed that human liver macrophages expressing CD14 and CD68 are highly responsive to IFN-$\lambda$ ex vivo. Together, these data highlight a novel role for macrophages in shaping IFN-$\lambda$ dependent immune responses both directly through pro-inflammatory activity and indirectly by recruiting and activating IFN-$\lambda$ unresponsive lymphocytes.

更多信息

更多信息
Species Mouse
Magnet Compatibility • EasySep™ Magnet (Catalog #18000) • “The Big Easy” EasySep™ Magnet (Catalog #18001) • EasyEights™ EasySep™ Magnet (Catalog #18103) • RoboSep™-S (Catalog #21000)
Sample Source Other, Spleen
Selection Method Positive
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