EasySep™小鼠B细胞分选试剂盒

通过免疫磁珠负选分离出无磁珠标记的小鼠B细胞

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¥9,144.00

产品号 #（选择产品）

产品号 #19854_C

通过免疫磁珠负选分离出无磁珠标记的小鼠B细胞

产品优势

易于操作、快速
纯度高达95%
无需分离柱
获得的活细胞无标记

产品组分包括

EasySep™小鼠B细胞分选试剂盒（产品号 #19854）

EasySep™小鼠B细胞分选抗体混合物，0.5 mL
EasySep™ Streptavidin RapidSpheres™ 50001磁珠，1 mL
EasySep™小鼠FcR阻断剂，0.2 mL

RoboSep™小鼠B细胞分选试剂盒（产品号 #19854RF）

EasySep™小鼠B细胞分选抗体混合物，0.5 mL
EasySep™ Streptavidin RapidSpheres™ 50001磁珠，1 mL
EasySep™小鼠FcR阻断剂，0.2 mL
RoboSep™ 缓冲液（产品号#20104）
RoboSep™过滤吸头（产品号#20125）

立即询价

总览

使用 EasySep™ 小鼠 B 细胞分离试剂盒，可通过免疫磁性负选法从脾细胞或其他组织样本的单细胞悬液中轻松高效地分离高纯度的小鼠 B 细胞。EasySep™ 技术在已发表研究中被广泛应用超过 20 年，结合了单克隆抗体的特异性与无柱磁系统的简便性。

在此 EasySep™ 负选步骤中，不需要的细胞通过抗体复合物和磁性颗粒进行标记。表达以下标志物的细胞将被去除：CD11b、CD4、CD8a、Ly6G/C、Ter119、CD43、CD49b 和 CD90.2。经 EasySep™ 磁体分离后，带有磁性标记的不需要细胞被去除，未标记的目标 B 细胞通过倾倒或移液方式转移至新试管中。磁性细胞分离最快可在 15 分钟内完成，目标 B 细胞可直接用于流式细胞术、培养及基于细胞的实验等下游应用。

如需分离表达 CD11b 或 CD43 的 B 细胞，建议使用 EasySep™ 小鼠全 B 细胞分离试剂盒（产品号#19844）。

了解更多关于 EasySep™ 免疫磁性技术的工作原理，或了解如何使用 RoboSep™ 实现免疫磁性细胞分离的全自动化。探索更多优化实验流程的产品，包括培养基、补充物、抗体等。

实验数据

Figure 1. Typical EasySep™ Mouse B Cell Isolation Profile

Starting with mouse splenocytes, the B cell content (CD19+CD3-) of the isolated fraction is 97.6 ± 1.7% (mean ± SD), using the purple EasySep™ Magnet.

Figure 2. EasySep™ Cell Isolation Protocol Lengths

Typical time taken (in minutes) to isolate cells using select EasySep™ kits.

产品说明书及文档

请在《产品说明书》中查找相关支持信息和使用说明，或浏览下方更多实验方案。

常见问题 (7)

Can EasySep™ Streptavidin RapidSpheres™ be used for either positive or negative selection?

Currently, EasySep™ Streptavidin RapidSphere™ kits are only available for negative selection and work by targeting and removing unwanted cells.

How does the separation work?

Streptavidin RapidSphere™ magnetic particles are crosslinked to unwanted cells using biotinylated antibodies. When placed in the EasySep™ Magnet, labeled cells migrate to the wall of the tube. The unlabeled cells are then poured off into a new tube.

Which columns do I use?

The EasySep™ procedure is column-free. That's right - no columns!

How can I analyze the purity of my enriched sample?

The Product Information Sheet provided with each EasySep™ kit contains detailed staining information.

Can EasySep™ Streptavidin RapidSphere™ separations be automated?

Yes. RoboSep™, the fully automated cell separator, automates all EasySep™ labeling and cell separation steps.

Are cells isolated using EasySep™ RapidSphere™ products FACS-compatible?

Yes. Desired cells are unlabeled and ready to use in downstream applications, such as FACS analysis.

Can I alter the separation time in the magnet?

Yes; however, this may impact the kit's performance. The provided EasySep™ protocols have already been optimized to balance purity, recovery and time spent on the isolation.

文献 (53)

PI3Kdelta-driven expansion of regulatory B cells impairs protective immune responses to Trypanosoma congolense parasite infection F. Olayinka-Adefemi et al. PLOS Pathogens 2025 Nov

Abstract

Phosphatidylinositol 3-kinase delta (PI3KCD) is a critical signaling enzyme for B cell development, activation, function and immune regulation. Gain-of-function mutations in PI3KCD result in the congenital immunodeficiency known as Activated PI3KCD Syndrome (APDS). APDS patients are prone to repeated infections and other serious clinical manifestations. Here, we determine how B cell-intrinsic expression of the APDS-associated PI3KCDE1021K mutation impacts immune responses to the protozoan parasite Trypanosoma congolense. PI3KCDE1021K/B mice exhibit a significant expansion of IL10-expressing B cells within the spleen and peritoneal cavity, which was associated with impaired control of T. congolense infection. Despite the generation of robust germinal center, plasma cell and antibody responses, PI3KCDE1021K/B mice show elevation in the first wave of parasitemia and increased mortality. We further characterize the phenotype of the expanded IL10-producing B cell population in PI3KCDE1021K/B mice, which show hallmarks of innate-like regulatory B cells (Breg) and expression of multiple inhibitory molecules. This Breg expansion is associated with reduced IFNγ/IL10 ratio, reduced TNFα production and impaired activation of myeloid cells, likely compromising the innate response to infection. These findings highlight the profound impact of dysregulated PI3KCD activity on regulatory B cells that can functionally impair innate immune responses controlling a systemic parasite protozoan disease. Author summaryB cells and antibodies play a critical role in the immune response to Trypanosome parasites. Molecular signaling networks within B cells can control the type of response generated during infection. Here, we studied how a genetic variant in the signaling enzyme PI3KCD, previously linked to human immune deficiencies, impacts B cell responses to Trypanosome infection. We find that mice expressing the PI3KCDE1021K mutation in their B cells show impaired control of Trypanosome infection, and alterations in several aspects of the immune response. Specifically, we noted these mice poorly control parasite growth within the first week of infection, a timeframe where specific antibody responses have not yet been generated. We noted an altered balance between pro-inflammatory and anti-inflammatory cytokine mediators produced within the first week of infection. This was associated with high numbers of regulatory B cells expressing multiple molecules capable of inhibiting other cells of the immune system. We further found that these mice show functional alterations in other critical immune cell types, such as macrophages and T cells. These findings highlight the impact of dysregulated PI3KCD activity on regulatory B cells that can impair immune responses controlling a systemic parasite protozoan disease.

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Sequences within and upstream of the mouse Ets1 gene drive high level expression in B cells, but are not sufficient for consistent expression in T cells PLOS One 2025 Mar

Abstract

The levels of transcription factor Ets1 are high in resting B and T cells, but are downregulated by signaling through antigen receptors and Toll-like receptors (TLRs). Loss of Ets1 in mice leads to excessive immune cell activation and development of an autoimmune syndrome and reduced Ets1 expression has been observed in human PBMCs in the context of autoimmune diseases. In B cells, Ets1 serves to prevent premature activation and differentiation to antibody-secreting cells. Given these important roles for Ets1 in the immune response, stringent control of Ets1 gene expression levels is required for homeostasis. However, the genetic regulatory elements that control expression of the Ets1 gene remain relatively unknown. Here we identify a topologically-associating domain (TAD) in the chromatin of B cells that includes the mouse Ets1 gene locus and describe an interaction hub that extends over 100 kb upstream and into the gene body. Additionally, we compile epigenetic datasets to find several putative regulatory elements within the interaction hub by identifying regions of high DNA accessibility and enrichment of active enhancer histone marks. Using reporter constructs, we determine that DNA sequences within this interaction hub are sufficient to direct reporter gene expression in lymphoid tissues of transgenic mice. Further analysis indicates that the reporter construct drives faithful expression of the reporter gene in mouse B cells, but variegated expression in T cells, suggesting the existence of T cell regulatory elements outside this region. To investigate how the downregulation of Ets1 transcription is associated with alterations in the epigenetic landscape of stimulated B cells, we performed ATAC-seq in resting and BCR-stimulated primary B cells and identified four regions within and upstream of the Ets1 locus that undergo changes in chromatin accessibility that correlate to Ets1 gene expression. Interestingly, functional analysis of several putative Ets1 regulatory elements using luciferase constructs suggested a high level of functional redundancy. Taken together our studies reveal a complex network of regulatory elements and transcription factors that coordinate the B cell-specific expression of Ets1.

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B cells are not drivers of stromal cell activation during acute CNS infection Journal of Neuroinflammation 2025 Jun

Abstract

BackgroundCNS stromal cells, especially fibroblasts and endothelial cells, support leukocyte accumulation through upregulation of adhesion molecules and lymphoid chemokines. While chronically activated fibroblast networks can drive pathogenic immune cell aggregates known as tertiary lymphoid structures (TLS), early stromal cell activation during CNS infection can support anti-viral T cells. However, the cell types and factors driving early stromal cell activation is poorly explored.AimsA neurotropic murine coronavirus (mCoV) infection model was used to better characterize signals that promote fibroblast networks supporting accumulation of antiviral lymphocytes. Based on the early appearance of IgD+ B cells with unknown functions during several CNS infections, we probed their potential to activate stromal cells through lymphotoxin β (LTβ), a molecule critical in maintaining fibroblast-networks in lymphoid tissues as well as promoting TLS in autoimmunity and cancers.ResultsKinetic analysis of stromal cell activation in olfactory bulbs and brains revealed that upregulation of adhesion molecules and lymphoid chemokines Ccl19, Ccl21 and Cxcl13 closely tracked viral replication. Immunohistochemistry revealed that upregulation of the fibroblast marker podoplanin (PDPN) at meningeal and perivascular sites mirrored kinetics of RNA expression. Moreover, both B cells and T cells colocalized to areas of PDPN reactivity, supporting a potential role in regulating stromal cell activation. However, specific depletion of LTβ from B cells using Mb1-creERT2 x Ltβfl/fl mice had no effect on T or B cell recruitment or viral replication. B cell depletion by anti-CD20 antibody also had no adverse effects. Surprisingly, LTβR agonism reduced viral control and parenchymal T cell localization despite increasing stromal cell lymphoid chemokines and PDPN. Additional assessment of direct stromal cell activation by the viral RNA mimic poly I:C showed induction of Pdpn and Ccl19 preceding Ltb.ConclusionsNeither B cell-derived LTβ or B cells are primary drivers of stromal cell activation networks in the CNS following mCoV infection. Although supplementary agonist mediated LTβR engagement confirmed a role for LTβ in enhancing PDPN and lymphoid chemokine expression, it impeded T cell migration to the CNS parenchyma and viral control. Our data overall indicate that stromal cells can integrate LTβR signals to tune their activation, but that LTβ is not necessarily essential and can even dysregulate protective antiviral T cell functions.Supplementary InformationThe online version contains supplementary material available at 10.1186/s12974-025-03491-7.

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更多信息

更多信息
物种	小鼠
Magnet Compatibility	• EasySep™ Magnet (Catalog #18000) • “The Big Easy” EasySep™ Magnet (Catalog #18001) • EasyPlate™ EasySep™ Magnet (Catalog 18102) • EasyEights™ EasySep™ Magnet (Catalog #18103) • RoboSep™-S (Catalog #21000)
样本来源	其它细胞系, 脾脏
Selection Method	Negative

EasySep™小鼠B细胞分选试剂盒

产品号 #19854

产品号 #19854RF

产品号 #（选择产品）

产品号 #19854_C

产品优势

产品组分包括

总览

实验数据

产品说明书及文档

应用领域

相关材料与文献

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Scientists Helping Scientists™

EasySep™小鼠B细胞分选试剂盒

产品号 #19854

产品号 #19854RF

产品号 #（选择产品）

产品号 #19854_C

产品优势

产品组分包括

总览

实验数据

产品说明书及文档

应用领域

相关材料与文献

技术资料 (11)

常见问题 (7)

Can EasySep™ Streptavidin RapidSpheres™ be used for either positive or negative selection?

How does the separation work?

Which columns do I use?

How can I analyze the purity of my enriched sample?

Can EasySep™ Streptavidin RapidSphere™ separations be automated?

Are cells isolated using EasySep™ RapidSphere™ products FACS-compatible?

Can I alter the separation time in the magnet?

文献 (53)

Abstract

Abstract

Abstract

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更多信息

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