EasySep™ Release Human CD19 Positive Selection Kit

Immunomagnetic positive selection kit using particle release technology
EasySep™ Release Human CD19 Positive Selection Kit

Immunomagnetic positive selection of particle-free human CD19+ cells

1 x 10^9 cells
Catalog # 17754
735 USD
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Required Products
  1. EasySep™ Magnet
    EasySep™ Magnet

    Magnet for column-free immunomagnetic separation

  2. EasySep™ Buffer
    EasySep™ Buffer

    Cell separation buffer

Overview

The EasySep™ Release Human CD19 Positive Selection Kit is designed to isolate CD19+ cells from fresh or previously frozen peripheral blood mononuclear cells or washed leukapheresis samples by immunomagnetic positive selection.

Desired cells are labeled with antibodies and magnetic particles, and separated without columns using an EasySep™ magnet. Unwanted cells are simply poured off, while desired cells remain in the tube. Then, bound magnetic particles are removed from the EasySep™-isolated CD19+ cells, which are immediately available for downstream applications. Following cell isolation with this EasySep™ Release kit, antibody complexes remain bound to the cell surface and may interact with Brilliant Violet™ antibody conjugates, polyethylene glycol-modified proteins or other chemically related ligands. The CD19 antigen is expressed on mature B cells and B cell progenitors but is lost upon maturation to plasma cells. It is also expressed on follicular dendritic cells.
Advantages
• Highly purified human CD19+ cells isolated in less than 30 minutes
• No-wash removal of EasySep™ Releasable RapidSpheres™
Components
  • EasySep™ Release Human CD19 Positive Selection Kit (Catalog #17754)
    • EasySep™ Release Human CD19 Positive Selection Cocktail, 1 mL
    • EasySep™ Releasable RapidSpheres™ 50201, 1 mL
    • EasySep™ Release Buffer (Concentrate), 3 x 1 mL
Magnet Compatibility
• EasySep™ Magnet (Catalog #18000)
• “The Big Easy” EasySep™ Magnet (Catalog #18001)
• EasyPlate™ Magnet (Catalog #18102)
• EasyEights™ Magnet (Catalog #18103)
Subtype
Cell Isolation Kits
Cell Type
B Cells
Species
Human
Sample Source
Leukapheresis, PBMC
Selection Method
Positive
Brand
EasySep
Area of Interest
Immunology

Scientific Resources

Product Documentation

Document Type Product Name Catalog # Lot # Language
Document Type
Product Information Sheet 1
Product Name
EasySep™ Release Human CD19 Positive Selection Kit
Catalog #
17754
Lot #
19D102116 or lower
Language
English
Document Type
Product Information Sheet 2
Product Name
EasySep™ Release Human CD19 Positive Selection Kit
Catalog #
17754
Lot #
1000006155 and higher
Language
English
Document Type
Safety Data Sheet 1
Product Name
EasySep™ Release Human CD19 Positive Selection Kit
Catalog #
17754
Lot #
All
Language
English
Document Type
Safety Data Sheet 2
Product Name
EasySep™ Release Human CD19 Positive Selection Kit
Catalog #
17754
Lot #
All
Language
English
Document Type
Safety Data Sheet 3
Product Name
EasySep™ Release Human CD19 Positive Selection Kit
Catalog #
17754
Lot #
All
Language
English

Educational Materials (9)

Brochure
EasySep™ Cell Separation Technology
Brochure
Human B Cell Isolation Product Selection
Brochure
Tools For Your Immunology Research
Brochure
EasySep™ Release Free Your Positively Selected Cells from Magnetic Particles
Wallchart
Frequencies of Cell Types in Human Peripheral Blood
Wallchart
Human Immune Cytokines
Video
Simultaneous Cell Isolation from Multiple Samples Using the EasyEights™ EasySep™ Magnet
0:57
Simultaneous Cell Isolation from Multiple Samples Using the EasyEights™ EasySep™ Magnet
Video
How EasySep™ Magnetic Cell Separation Technology Works: Fast and Easy Cell Isolation
1:57
How EasySep™ Magnetic Cell Separation Technology Works: Fast and Easy Cell Isolation
Scientific Poster
Releasable RapidSpheres Enable Immunomagnetic Purification of Highly Viable and Functional Immune Cells from Complex Tissues in Less Than 30 Minutes

Product 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.

Data and Publications

Data

Starting with a single-cell suspension of human PBMCs, the CD19+ cell content of the isolated fraction is typically 97.7 ± 2.3% (mean ± SD using the purple EasySep™ Magnet). In the above example, the purities of the start and final isolated fractions are 6.2% and 98.0%, respectively.

Publications (3)

Science advances 2020 oct Leukemia-on-a-chip: Dissecting the chemoresistance mechanisms in B cell acute lymphoblastic leukemia bone marrow niche. C. Ma et al.

Abstract

B cell acute lymphoblastic leukemia (B-ALL) blasts hijack the bone marrow (BM) microenvironment to form chemoprotective leukemic BM niches facilitating chemoresistance and, ultimately, disease relapse. However, the ability to dissect these evolving, heterogeneous interactions among distinct B-ALL subtypes and their varying BM niches is limited with current in vivo methods. Here, we demonstrated an in vitro organotypic leukemia-on-a-chip" model to emulate the in vivo B-ALL BM pathology and comparatively studied the spatial and genetic heterogeneity of the BM niche in regulating B-ALL chemotherapy resistance. We revealed the heterogeneous chemoresistance mechanisms across various B-ALL cell lines and patient-derived samples. We showed that the leukemic perivascular endosteal and hematopoietic niche-derived factors maintain B-ALL survival and quiescence (e.g. CXCL12 cytokine signal VCAM-1/OPN adhesive signals and enhanced downstream leukemia-intrinsic NF-$\kappa$B pathway). Furthermore we demonstrated the preclinical use of our model to test niche-cotargeting regimens which may translate to patient-specific therapy screening and response prediction."
Frontiers in immunology 2020 Fli1 Downregulation in Scleroderma Myeloid Cells Has Profibrotic and Proinflammatory Effects. A. M. Bujor et al.

Abstract

Scleroderma (SSc) is an autoimmune connective tissue disease characterized by immune dysregulation, vasculopathy, and fibrosis. We have previously demonstrated that low Fli1 expression in SSc fibroblasts and endothelial cells plays an important role in SSc pathogenesis. Cells of myeloid and lymphoid origin also express Fli1 and are dysregulated in patients with SSc, playing key roles in disease pathogenesis. However, the role for immune Fli1 in SSc is not yet clear. Our aim was to elucidate whether Fli1 contributes to the immune dysregulation seen in SSc. Comparison of the expression of Fli1 in monocytes, B- and T-cell fractions of PBMCs isolated from SSc patients and healthy controls (HC), showed an increase in Fli1 levels in monocytes. We used siRNA transfected human myeloid cells and mouse peritoneal macrophages obtained from Fli1 flox/flox LysMCre+/+ mice, and found that markers of alternative macrophage activation were increased with Fli1 deletion. Coculture of Fli1-deficient myeloid cells and primary human or mouse fibroblasts resulted in a potent induction of collagen type I, independent of TGF$\beta$ upregulation. We next analyzed global gene expression profile in response to Fli1 downregulation, to gain further insight into the molecular mechanisms of this process and to identify differentially expressed genes in myeloid cells. Of relevance to SSc, the top most upregulated pathways were hallmark IFN-$\gamma$ and IFN-$\alpha$ response. Additionally, several genes previously linked to SSc pathogenesis and fibrosis in general were also induced, including CCL2, CCL7, MMP12, and CXCL10. ANKRD1, a profibrotic transcription co-regulator was the top upregulated gene in our array. Our results show that Fli1-deficient myeloid cells share key features with cells from SSc patients, with higher expression of profibrotic markers and activation of interferon responsive genes, thus suggesting that dysregulation of Fli1 in myeloid cells may contribute to SSc pathogenesis.
Acta neuropathologica communications 2017 dec CRISPR/Cas9-Correctable mutation-related molecular and physiological phenotypes in iPSC-derived Alzheimer's PSEN2 N141I neurons. M. Ortiz-Virumbrales et al.

Abstract

Basal forebrain cholinergic neurons (BFCNs) are believed to be one of the first cell types to be affected in all forms of AD, and their dysfunction is clinically correlated with impaired short-term memory formation and retrieval. We present an optimized in vitro protocol to generate human BFCNs from iPSCs, using cell lines from presenilin 2 (PSEN2) mutation carriers and controls. As expected, cell lines harboring the PSEN2 N141I mutation displayed an increase in the A$\beta$42/40 in iPSC-derived BFCNs. Neurons derived from PSEN2 N141I lines generated fewer maximum number of spikes in response to a square depolarizing current injection. The height of the first action potential at rheobase current injection was also significantly decreased in PSEN2 N141I BFCNs. CRISPR/Cas9 correction of the PSEN2 point mutation abolished the electrophysiological deficit, restoring both the maximal number of spikes and spike height to the levels recorded in controls. Increased A$\beta$42/40 was also normalized following CRISPR/Cas-mediated correction of the PSEN2 N141I mutation. The genome editing data confirms the robust consistency of mutation-related changes in A$\beta$42/40 ratio while also showing a PSEN2-mutation-related alteration in electrophysiology.
View All Publications

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