RoboSep™-S

RoboSep™-S - The Fully Automated Cell Separator
RoboSep™-S

RoboSep™-S - The Fully Automated Cell Separator

1 Unit
Catalog # 21000
RoboSep™ Tube Kit (9 Plastic Tubes + Tip Head Protector)

RoboSep™ tube kit

1 Kit
Catalog # 20155
8 USD
RoboSep™ Tip Head Polishing Compound

RoboSep™ support reagent

7 mL
Catalog # 20119
63 USD
New look, same high quality and support! You may notice that your instrument or reagent packaging looks slightly different from images displayed on the website, or from previous orders. We are updating our look but rest assured, the products themselves and how you should use them have not changed. Learn more
Required Products
  1. RoboSep™ Buffer
    RoboSep™ Buffer

    Cell separation buffer

  2. RoboSep™ Tip Head Polishing Compound
    RoboSep™ Tip Head Polishing Compound

    RoboSep™ support reagent

  3. RoboSep™ Filter Tips
    RoboSep™ Filter Tips

    RoboSep™ accessories

  4. RoboSep™-S|21000
    RoboSep™-S Additional Service Packages

    RoboSep™-S - The Fully Automated Cell Separator

Overview

RoboSep™-S is the next-generation RoboSep™ instrument for fully automated cell separation. Using EasySep™ technology, RoboSep™-S performs all steps necessary to magnetically label and separate virtually any cell type by positive or negative selection. RoboSep™-S is designed to minimize sample handling, eliminate cross-contamination, and reduce “hands-on” time.

To view cell isolation kits for use with RoboSep™-S, visit our Cell Isolation Products page.

Leasing options and warranty coverage are available. Please contact us for further information.

For more information about Instrument Services including additional service packages and software please see our instrumentation overview.
Contains
• RoboSep™-S Base Unit (Catalog #21001)
• "The Big Easy" EasySep™ Magnets (Catalog #18001)
• RoboSep™ Service Rack (Catalog #20101)
• RoboSep™ Tube Kits (Catalog #20155)
• USB Flash Drive
• RoboSep™ User Reference Manual (Catalog #29792)
• RoboSep™ Quick Start Guide (Catalog #28943)
• 1-Year Warranty (Catalog #21200)
Species
Human, Mouse, Rat, Non-Human Primate, Other
Application
Cell Isolation
Brand
RoboSep
Area of Interest
Chimerism, HLA, Immunology, Stem Cell Biology

Scientific Resources

Product Documentation

Document Type Product Name Catalog # Lot # Language
Document Type
Product Information Sheet
Product Name
RoboSep™ Tip Head Polishing Compound
Catalog #
20119
Lot #
All
Language
English
Document Type
Manual
Product Name
RoboSep™-S
Catalog #
21000
Lot #
All
Language
English
Document Type
Safety Data Sheet
Product Name
RoboSep™ Tip Head Polishing Compound
Catalog #
20119
Lot #
All
Language
English

Educational Materials (26)

Brochure
Instrument Service
Brochure
Cell Separation Products for HLA Analysis
Brochure
Mouse Cell Isolation
Brochure
Fully Automated Cell Isolation with RoboSep™
Brochure
RoboSep™-S Quick Start Procedure
Technical Bulletin
Enhance Sensitivity of Multiple Myeloma Testing with Purified CD138 Plasma Cells
Technical Bulletin
Purity Assessment by Flow Cytometry for Lineage-Specific Chimerism Analysis
Technical Bulletin
Fully Automated, High Purity Cell Isolation for Chimerism Labs
Wallchart
Human Immune Cytokines
Wallchart
The Immune Response to HIV Poster
Video
Considerations to Streamline the Flow Cytometry Crossmatch (FCXM) Assay
29:55
Considerations to Streamline the Flow Cytometry Crossmatch (FCXM) Assay
Video
Automate Cell Isolation with the RoboSep™-S Cell Separation Instrument
1:41
Automate Cell Isolation with the RoboSep™-S Cell Separation Instrument
Webinar
Online Immunology Journal Club: Expanding the Therapeutic Tool Kit for CAR T Cells
47:14
Online Immunology Journal Club: Expanding the Therapeutic Tool Kit for CAR T Cells
Webinar
Fully Automated Cell Separation for Chimerism Analysis with RoboSep™
56:02
Fully Automated Cell Separation for Chimerism Analysis with RoboSep™
Webinar
T Cell Differentiation and Cancer Immunity
48:32
T Cell Differentiation and Cancer Immunity
Scientific Poster
Isolation of CD19, CD3 and Myeloid Cells from one Tube of Whole Blood
Scientific Poster
Isolation of Eosinophils Without Ficoll or RBC Lysis
Scientific Poster
Pre-Enrichment of Dendritic Cells from Human Peripheral Blood Samples
Scientific Poster
Cell Isolation of Human CD4+ Memory T Cells By Column-Free Immunomagnetic Cell Separation
Scientific Poster
Cell Isolation of Highly Purified Monocytes Using Fully Automated Negative Cell Selection
Scientific Poster
Rapid, Automated Lymphocyte Isolation Directly from Whole Blood with EasySep™ Direct
Scientific Poster
Method for Negative Enrichment of Monocytes from Mouse Blood and Bone Marrow
Scientific Poster
Isolation of Human Regulatory T Cells from Peripheral Blood Samples
Scientific Poster
Isolation of Plasmacytoid Dendritic Cells from Human Peripheral Blood
Scientific Poster
Procedure for Negative Enrichment of Monocytes from Mouse Blood and Bone Marrow
Scientific Poster
Cell Enrichment of Specific Lymphocyte Populations (T Cells, B Cells, Total Lymphocytes) from Whole Blood
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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

Publications (63)

Leukemia 2019 mar Selective targeting of multiple myeloma by B cell maturation antigen (BCMA)-specific central memory CD8+ cytotoxic T lymphocytes: immunotherapeutic application in vaccination and adoptive immunotherapy. J. Bae et al.

Abstract

To expand the breadth and extent of current multiple myeloma (MM)-specific immunotherapy, we have identified various antigens on CD138+ tumor cells from newly diagnosed MM patients (n = 616) and confirmed B-cell maturation antigen (BCMA) as a key myeloma-associated antigen. The aim of this study is to target the BCMA, which promotes MM cell growth and survival, by generating BCMA-specific memory CD8+ CTL that mediate effective and long-lasting immunity against MM. Here we report the identification of novel engineered peptides specific to BCMA, BCMA72-80 (YLMFLLRKI), and BCMA54-62 (YILWTCLGL), which display improved affinity/stability to HLA-A2 compared to their native peptides and induce highly functional BCMA-specific CTL with increased activation (CD38, CD69) and co-stimulatory (CD40L, OX40, GITR) molecule expression. Importantly, the heteroclitic BCMA72-80 specific CTL demonstrated poly-functional Th1-specific immune activities [IFN-gamma/IL-2/TNF-alpha production, proliferation, cytotoxicity] against MM, which were correlated with expansion of Tetramer+ and memory CD8+ CTL. Additionally, heteroclitic BCMA72-80 specific CTL treated with anti-OX40 (immune agonist) or anti-LAG-3 (checkpoint inhibitor) display increased immune function, mainly by central memory CTL. These results provide the framework for clinical application of heteroclitic BCMA72-80 peptide, alone and in combination with anti-LAG3 and/or anti-OX40 therapy, in vaccination and/or adoptive immunotherapeutic strategies to generate long-lasting anti-tumor immunity in patients with MM or other BCMA expressing tumors.
Nature metabolism 2019 jul Metabolic plasticity of HIV-specific CD8+ T cells is associated with enhanced antiviral potential and natural control of HIV-1 infection. M. Angin et al.

Abstract

Spontaneous control of human immunodeficiency virus (HIV) is generally associated with an enhanced capacity of CD8+ T cells to eliminate infected CD4+ T cells, but the molecular characteristics of these highly functional CD8+ T cells are largely unknown. In the present study, using single-cell analysis, it was shown that HIV-specific, central memory CD8+ T cells from spontaneous HIV controllers (HICs) and antiretrovirally treated non-controllers have opposing transcriptomic profiles. Genes linked to effector functions and survival are upregulated in cells from HICs. In contrast, genes associated with activation, exhaustion and glycolysis are upregulated in cells from non-controllers. It was shown that HIV-specific CD8+ T cells from non-controllers are largely glucose dependent, whereas those from HICs have more diverse metabolic resources that enhance both their survival potential and their capacity to develop anti-HIV effector functions. The functional efficiency of the HIV-specific CD8+ T cell response in HICs is thus engraved in their memory population and related to their metabolic programme. Metabolic reprogramming in vitro through interleukin-15 treatment abrogated the glucose dependency and enhanced the antiviral potency of HIV-specific CD8+ T cells from non-controllers.
Immunity, inflammation and disease 2019 Complexin 2 regulates secretion of immunoglobulin in antibody-secreting cells. E. Tsuru et al.

Abstract

INTRODUCTION Complexins (CPLXs), initially identified in neuronal presynaptic terminals, are cytoplasmic proteins that interact with the soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNARE) complex to regulate the fusion of vesicles to the plasma membrane. Although much is known about CPLX function in neuronal synaptic vesicle exocytosis, their distribution and role in immune cells are still unclear. In this study, we investigated CPLX2 knockout (KO) mice to reveal the role of CPLXs in exocytosis of lymphocytes. METHODS We examined the expression of CPLXs and SNAREs in lymphocytes. To study the effect of CPLXs on the immune system in vivo, we analyzed the immune phenotype of CPLX2 KO mice. Furthermore, antibodies secretion from the peritoneal cavity, spleen, and bone marrow cells of wild-type (WT) and CPLX2 KO mice were determined. RESULTS CPLX2 was detected in B cells but not in T cells, while other CPLXs and SNAREs were expressed at a similar level in both B and T cells. To clarify the function of CPLX2 in B lymphocytes, serum concentrations of immunoglobulin G (IgG), IgA, IgM, and IgE were measured in WT and CPLX2 KO mice using enzyme-linked immunosorbent assay. The level of IgM, which mainly consists of natural antibodies, was higher in KO mice than that in WT mice, while the levels of other antibodies were similar in both types of mice. Additionally, we found that spontaneous secretion of IgM and IgG1 was enhanced from the splenic antibody-secreting cells (ASCs) of CPLX2 KO mice. CONCLUSION Our data suggest that CPLX2 inhibits spontaneous secretion of IgM and IgG1 from splenic ASCs. This study provides new insight into the mechanism of antibody secretion of ASCs.
The American journal of surgical pathology 2018 JUL PD-1 Expression in Chronic Lymphocytic Leukemia/Small Lymphocytic Lymphoma (CLL/SLL) and Large B-cell Richter Transformation (DLBCL-RT): A Characteristic Feature of DLBCL-RT and Potential Surrogate Marker for Clonal Relatedness. R. He et al.

Abstract

Chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL) is a low-grade B-cell neoplasm and ∼2{\%} to 9{\%} patients develop an aggressive lymphoma, most commonly diffuse large B-cell lymphoma (Richter transformation, DLBCL-RT). Programmed death-1 (PD-1) pathway plays a crucial role in tumor host immunity evasion and its blockade has emerged as an effective anti-cancer immunotherapy. PD-L1 and PD-1 expression has shown predictive value in anti-PD cancer immunotherapy; however, it has not been well documented in CLL/SLL and DLBCL-RT. We evaluated PD-1 and PD-L1 expression by immunohistochemistry in 39 CLL/SLL, 15 DLBCL-RT, and 26 other DLBCL. In CLL/SLL, neoplastic B-cell PD-1 expression was weak and restricted to prolymphocytes/paraimmunoblasts within proliferation centers (PCs) and accentuated PCs of all sizes. Neoplastic B-cell PD-1 expression was highly prevalent and demonstrated increased intensity in DLBCL-RT, but in contrast was only rarely seen in other DLBCL (12/15 vs. 1/26; P{\textless}0.0001). An excellent correlation (90{\%} concordance) was observed between neoplastic B-cell PD-1 immunohistochemistry positivity and molecularly defined CLL/SLL clonal relatedness in DLBCL-RT. PD-L1 expression was observed on the neoplastic B cells in rare DLBCL-RT and other DLBCL cases (1/15 vs. 1/26; P{\textgreater}0.05) as well as background histiocytes and dendritic cells. Overall survival of DLBCL-RT was significantly inferior to that of the other DLBCL (median, 16.9 vs. 106.1 mo; P=0.002). Our findings suggest a biological continuum from prolymphocytes/paraimmunoblasts in CLL/SLL PCs to the neoplastic B-cells in DLBCL-RT. The characteristic PD-1 expression in DLBCL-RT makes it a potential surrogate marker for determining clonal relatedness to CLL/SLL, which may have important prognostic and therapeutic implications.
Cancer genetics 2018 DEC Assessing genome-wide copy number aberrations and copy-neutral loss-of-heterozygosity as best practice: An evidence-based review from the Cancer Genomics Consortium working group for plasma cell disorders. T. J. Pugh et al.

Abstract

BACKGROUND Plasma cell neoplasms (PCNs) encompass a spectrum of disorders including monoclonal gammopathy of undetermined significance, smoldering myeloma, plasma cell myeloma, and plasma cell leukemia. Molecular subtypes have been defined by recurrent cytogenetic abnormalities and somatic mutations that are prognostic and predictive. Karyotype and fluorescence in situ hybridization (FISH) have historically been used to guide management; however, new technologies and markers raise the need to reassess current testing algorithms. METHODS We convened a panel of representatives from international clinical laboratories to capture current state-of-the-art testing from published reports and to put forward recommendations for cytogenomic testing of plasma cell neoplasms. We reviewed 65 papers applying FISH, chromosomal microarray (CMA), next-generation sequencing, and gene expression profiling for plasma cell neoplasm diagnosis and prognosis. We also performed a survey of our peers to capture current laboratory practice employed outside our working group. RESULTS Plasma cell enrichment is widely used prior to FISH testing, most commonly by magnetic bead selection. A variety of strategies for direct, short- and long-term cell culture are employed to ensure clonal representation for karyotyping. Testing of clinically-informative 1p/1q, del(13q) and del(17p) are common using karyotype, FISH and, increasingly, CMA testing. FISH for a variety of clinically-informative balanced IGH rearrangements is prevalent. Literature review found that CMA analysis can detect abnormalities in 85-100{\%} of patients with PCNs; more specifically, in 5-53{\%} (median 14{\%}) of cases otherwise normal by FISH and cytogenetics. CMA results in plasma cell neoplasms are usually complex, with alteration counts ranging from 1 to 74 (median 10-20), primarily affecting loci not covered by FISH testing. Emerging biomarkers include structural alterations of MYC as well as somatic mutations of KRAS, NRAS, BRAF, and TP53. Together, these may be measured in a comprehensive manner by a combination of newer technologies including CMA and next-generation sequencing (NGS). Our survey suggests most laboratories have, or are soon to have, clinical CMA platforms, with a desire to move to NGS assays in the future. CONCLUSION We present an overview of current practices in plasma cell neoplasm testing as well as an algorithm for integrated FISH and CMA testing to guide treatment of this disease.
Scientific reports 2017 JAN Non-pathogenic tissue-resident CD8+ T cells uniquely accumulate in the brains of lupus-prone mice. P. A. Morawski et al.

Abstract

Severe lupus often includes psychiatric and neurological sequelae, although the cellular contributors to CNS disease remain poorly defined. Using intravascular staining to discriminate tissue-localized from blood-borne cells, we find substantial accumulation of CD8+ T cells relative to other lymphocytes in brain tissue, which correlates with lupus disease and limited neuropathology. This is in contrast to all other affected organs, where infiltrating CD4+ cells are predominant. Brain-infiltrating CD8+ T cells represent an activated subset of those found in the periphery, having a resident-memory phenotype (CD69+CD122-PD1+CD44+CD62L-) and expressing adhesion molecules (VLA-4+LFA-1+) complementary to activated brain endothelium. Remarkably, infiltrating CD8+ T cells do not cause tissue damage in lupus-prone mice, as genetic ablation of these cells via $\beta$2 m deficiency does not reverse neuropathology, but exacerbates disease both in the brain and globally despite decreased serum IgG levels. Thus, lupus-associated inflammation disrupts the blood-brain barrier in a discriminating way biased in favor of non-pathogenic CD8+ T cells relative to other infiltrating leukocytes, perhaps preventing further tissue damage in such a sensitive organ.
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