SepMate™-15 (IVD)

Tube for density gradient centrifugation for in vitro diagnostic (IVD) applications

Try SepMate™-15 (IVD) tubes for density gradient centrifugation in your IVD applications. Request a Sample

SepMate™-15 (IVD)

Tube for density gradient centrifugation for in vitro diagnostic (IVD) applications

From: 413 USD
Catalog #
85415_C
Tube for density gradient centrifugation for in vitro diagnostic (IVD) applications

Product Advantages


  • Eliminates the need for carefully layering blood over the density gradient medium (e.g. Lymphoprep™, etc.)

  • Reduces total centrifuge time to 10 minutes with the brake on for fresh samples

  • Allows fast and easy harvesting of the isolated mononuclear cells by simply pouring off the supernatant

  • Can be combined with RosetteSep™ enrichment cocktails to isolate specific cell types in just 30 minutes

What's Included

  • SepMate™-15 (IVD), 100 Tubes (Catalog #85415)
    • Dispenser box containing 4 bags, 25 Tubes/Bag
  • SepMate™-15 (IVD), 500 Tubes (Catalog #85420)
    • Dispenser box containing 4 bags, 25 Tubes/Bag (Catalog #85415) x 5
Try SepMate™-15 (IVD) tubes for density gradient centrifugation in your IVD applications. Request a Sample
Products for Your Protocol

What Our Scientist Says

Traditional isolation of PBMCs requires careful layering of blood onto density gradient media prior to centrifugation. We developed SepMate™ to simplify this process, so anyone can isolate PBMCs with a simple pour while maintaining consistency across samples.

Peter MorinTechnical Scientist
Peter Morin, Technical Scientist

Overview

Simplify peripheral blood mononuclear cell (PBMC) isolation by incorporating SepMate™ into your density gradient centrifugation step.

SepMate™ tubes contain an insert that creates a barrier between the density gradient medium and blood, thus eliminating the need for careful blood layering and allowing mononuclear cells to be easily harvested with a simple pour. This product can be used with RosetteSep™ to isolate specific immune cell subsets.

SepMate™ is manufactured under cGMP and registered as an In Vitro Diagnostic (IVD) device in Australia, Canada, Europe, and the USA. In China, SepMate™ is considered a nonmedical device by the China Food and Drug Administration (CFDA) and should be used as general lab equipment. The end user is responsible for determining whether the product is suitable for their specific application.
Contains
Polypropylene tube containing an insert
Subtype
Centrifugation Tubes
Cell Type
B Cells, Dendritic Cells, Monocytes, Mononuclear Cells, NK Cells, T Cells, T Cells, CD4+, T Cells, CD8+, T Cells, Other Subsets, T Cells, Regulatory
Species
Human
Sample Source
Bone Marrow, Whole Blood
Selection Method
Negative
Application
Cell Isolation, In Vitro Diagnostic
Brand
SepMate
Area of Interest
Chimerism, HLA, Immunology

Data Figures

PBMC recovery from fresh whole blood using SepMate™-50 versus standard density gradient centrifugation. Graph also shows PBMC recovery from a 48 hour-old sample using SepMate™. n in each group = 7

Figure 1. Recovery of mononuclear cells (MNCs) from peripheral blood using SepMate™-50 versus standard density gradient centrifiguation.

Recovery of MNCs from fresh and 48-hour post blood draw enriched by density gradient centrifugation with SepMate™ (purple) or without (grey). There was no significant difference in the recovery of MNCS with and without SepMate™.

PBMC recovery from fresh whole blood using SepMate™-50 versus standard density gradient centrifugation. Graph also shows PBMC recovery from a 48 hour-old sample using SepMate™. n in each group = 7

Figure 2. Human CD4+ T Cell Isolation using SepMate™-50 and RosetteSep™ Human CD4+ T Cell Enrichment Cocktail

Protocols and Documentation

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

Document Type
Product Name
Catalog #
Lot #
Language
Catalog #
85415, 85420
Lot #
399999 and lower
Language
English
Catalog #
85415, 85420
Lot #
400000 and higher
Language
English

Resources and Publications

Publications (30)

A highly potent lymphatic system-targeting nanoparticle cyclosporine prevents glomerulonephritis in mouse model of lupus. R. Ganugula et al. Science advances 2020 jun

Abstract

Cyclosporine A (CsA) is a powerful immunosuppressant, but it is an ineffective stand-alone treatment for systemic lupus erythematosus (SLE) due to poor target tissue distribution and renal toxicity. We hypothesized that CD71 (transferrin receptor 1)-directed delivery of CsA to the lymphatic system would improve SLE outcomes in a murine model. We synthesized biodegradable, ligand-conjugated nanoparticles [P2Ns-gambogic acid (GA)] targeting CD71. GA conjugation substantially increased nanoparticle association with CD3+ or CD20+ lymphocytes and with intestinal lymphoid tissues. In orally dosed MRL-lpr mice, P2Ns-GA-encapsulated CsA increased lymphatic drug delivery 4- to 18-fold over the ligand-free formulation and a commercial CsA capsule, respectively. Improved lymphatic bioavailability of CsA was paralleled by normalization of anti-double-stranded DNA immunoglobulin G titer, plasma cytokines, and glomerulonephritis. Thus, this study demonstrates the translational potential of nanoparticles that enhance the targeting of lymphatic tissues, transforming CsA into a potent single therapeutic for SLE.
Longitudinal immune profiling reveals key myeloid signatures associated with COVID-19. E. R. Mann et al. Science immunology 2020

Abstract

COVID-19 pathogenesis is associated with an exaggerated immune response. However, the specific cellular mediators and inflammatory components driving diverse clinical disease outcomes remain poorly understood. We undertook longitudinal immune profiling on both whole blood and peripheral blood mononuclear cells (PBMCs) of hospitalized patients during the peak of the COVID-19 pandemic in the UK. Here, we report key immune signatures present shortly after hospital admission that were associated with the severity of COVID-19. Immune signatures were related to shifts in neutrophil to T cell ratio, elevated serum IL-6, MCP-1 and IP-10, and most strikingly, modulation of CD14+ monocyte phenotype and function. Modified features of CD14+ monocytes included poor induction of the prostaglandin-producing enzyme, COX-2, as well as enhanced expression of the cell cycle marker Ki-67. Longitudinal analysis revealed reversion of some immune features back to the healthy median level in patients with a good eventual outcome. These findings identify previously unappreciated alterations in the innate immune compartment of COVID-19 patients and lend support to the idea that therapeutic strategies targeting release of myeloid cells from bone marrow should be considered in this disease. Moreover, they demonstrate that features of an exaggerated immune response are present early after hospital admission suggesting immune-modulating therapies would be most beneficial at early timepoints.
A dominant autoinflammatory disease caused by non-cleavable variants of RIPK1 P. Tao et al. Nature 2020

Abstract

Activation of RIPK1 controls TNF-mediated apoptosis, necroptosis and inflammatory pathways1. Cleavage of human and mouse RIPK1 after residues D324 and D325, respectively, by caspase-8 separates the RIPK1 kinase domain from the intermediate and death domains. The D325A mutation in mouse RIPK1 leads to embryonic lethality during mouse development2,3. However, the functional importance of blocking caspase-8-mediated cleavage of RIPK1 on RIPK1 activation in humans is unknown. Here we identify two families with variants in RIPK1 (D324V and D324H) that lead to distinct symptoms of recurrent fevers and lymphadenopathy in an autosomal-dominant manner. Impaired cleavage of RIPK1 D324 variants by caspase-8 sensitized patients' peripheral blood mononuclear cells to RIPK1 activation, apoptosis and necroptosis induced by TNF. The patients showed strong RIPK1-dependent activation of inflammatory signalling pathways and overproduction of inflammatory cytokines and chemokines compared with unaffected controls. Furthermore, we show that expression of the RIPK1 mutants D325V or D325H in mouse embryonic fibroblasts confers not only increased sensitivity to RIPK1 activation-mediated apoptosis and necroptosis, but also induction of pro-inflammatory cytokines such as IL-6 and TNF. By contrast, patient-derived fibroblasts showed reduced expression of RIPK1 and downregulated production of reactive oxygen species, resulting in resistance to necroptosis and ferroptosis. Together, these data suggest that human non-cleavable RIPK1 variants promote activation of RIPK1, and lead to an autoinflammatory disease characterized by hypersensitivity to apoptosis and necroptosis and increased inflammatory response in peripheral blood mononuclear cells, as well as a compensatory mechanism to protect against several pro-death stimuli in fibroblasts.

Contact STEMCELL Technologies

Our Customer Service, Sales, and Product and Scientific Support departments in North America are available between 6 am and 5 pm Pacific Time (9 am and 8 pm Eastern Time). One of our representatives will be happy to help you by telephone or email. Please complete the form to contact us by email. A representative will get back to you shortly.
  •  

StemCell Technologies Inc. and affiliates ("STEMCELL Technologies") does not share your email address with third parties. StemCell Technologies Inc. will use your email address to confirm your identity and send you newsletters, transaction-related emails, promotional and customer service emails in accordance with our privacy policy. You can change your email preferences at any time.