Density gradient medium for the isolation of mononuclear cells

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Density gradient medium for the isolation of mononuclear cells
From: 86 USD


Lymphoprep™ is a density gradient medium recommended for the isolation of mononuclear cells from peripheral blood, cord blood, and bone marrow by exploiting differences in cell density. Granulocytes and erythrocytes have a higher density than mononuclear cells and therefore sediment through the Lymphoprep™ layer during centrifugation. Lymphoprep™ can be substituted for Ficoll-Paque™ without any need to change your existing protocols and is fully compatible with both SepMate™ and RosetteSep™ .

Lymphoprep™ has a density of 1.077 g/mL.
• Sodium diatrizoate (9.1% w/v)
• Polysaccharide (5.7% w/v)
• Other ingredients
Density Gradient Media
Cell Type:
Mononuclear Cells
Sample Source:
Bone Marrow; Cord Blood; Whole Blood
Selection Method:
Cell Isolation
Area of Interest:

Scientific Resources

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Data and Publications


Figure 1. Purity and Recovery of Cells from Whole Blood When Using Cost-Effective Lymphoprep™ is Comparable to Using Ficoll-Paque™ PLUS

(A) Density gradient centrifugation of peripheral whole blood using Lymphoprep™ results in similar cell purity of mononuclear cells including T cells, B cells, NK cells and monocytes compared to Ficoll-Paque™ PLUS. (B) The recovery of total mononuclear cells and CD45+ cells is also similar. (n = 5, Mean ± SD).

Figure 2. Purity and Recovery of Cells from Cord Blood When Using Cost-Effective Lymphoprep™ is Comparable to Using Ficoll-Paque™ PLUS

(A) Density Gradient centrifugation of cord blood using Lymphoprep™ results in similar cell purity of mononuclear cells including T cells, B cells, NK cells and monocytes compared to Ficoll-Paque™ PLUS. (B) The recovery of total mononuclear cells and CD45+ cells is also similar. (n = 4, Mean ± SD).


Scientific reports 2019 nov

Extracellular Membrane Vesicles from Lactobacilli Dampen IFN-$\gamma$ Responses in a Monocyte-Dependent Manner.

M. Mata Forsberg et al.


Secreted factors derived from Lactobacillus are able to dampen pro-inflammatory cytokine responses. Still, the nature of these components and the underlying mechanisms remain elusive. Here, we aimed to identify the components and the mechanism involved in the Lactobacillus-mediated modulation of immune cell activation. PBMC were stimulated in the presence of the cell free supernatants (CFS) of cultured Lactobacillus rhamnosus GG and Lactobacillus reuteri DSM 17938, followed by evaluation of cytokine responses. We show that lactobacilli-CFS effectively dampen induced IFN-$\gamma$ and IL-17A responses from T- and NK cells in a monocyte dependent manner by a soluble factor. A proteomic array analysis highlighted Lactobacillus-induced IL-1 receptor antagonist (ra) as a potential candidate responsible for the IFN-$\gamma$ dampening activity. Indeed, addition of recombinant IL-1ra to stimulated PBMC resulted in reduced IFN-$\gamma$ production. Further characterization of the lactobacilli-CFS revealed the presence of extracellular membrane vesicles with a similar immune regulatory activity to that observed with the lactobacilli-CFS. In conclusion, we have shown that lactobacilli produce extracellular MVs, which are able to dampen pro-inflammatory cytokine responses in a monocyte-dependent manner.
Scientific reports 2019 jan

Epstein-Barr Virus Latent Membrane Protein-1 Induces the Expression of SUMO-1 and SUMO-2/3 in LMP1-positive Lymphomas and Cells.

S. Salahuddin et al.


Epstein-Barr Virus latent membrane protein-1 (LMP1) interacts with the SUMO-conjugating enzyme Ubc9, which induces protein sumoylation and may contribute to LMP1-mediated oncogenesis. After analyzing human lymphoma tissues and EBV-positive cell lines, we now document a strong correlation between LMP1 and sumo-1/2/3 or SUMO-1/2/3 levels, and show that LMP1-induced sumo expression requires the activation of NF-kappaB signaling through CTAR1 and CTAR2. Together, these results point to a second mechanism by which LMP1 dysregulates sumoylation processes and adds EBV-associated lymphomas to the list of malignancies associated with increased SUMO expression.
Nature communications 2018 NOV

Cellular metabolism constrains innate immune responses in early human ontogeny.

B. Kan et al.


Pathogen immune responses are profoundly attenuated in fetuses and premature infants, yet the mechanisms underlying this developmental immaturity remain unclear. Here we show transcriptomic, metabolic and polysome profiling and find that monocytes isolated from infants born early in gestation display perturbations in PPAR-$\gamma$-regulated metabolic pathways, limited glycolytic capacity and reduced ribosomal activity. These metabolic changes are linked to a lack of translation of most cytokines and of MALT1 signalosome genes essential to respond to the neonatal pathogen Candida. In contrast, they have little impact on house-keeping phagocytosis functions. Transcriptome analyses further indicate a role for mTOR and its putative negative regulator DNA Damage Inducible Transcript 4-Like in regulating these metabolic constraints. Our results provide a molecular basis for the broad susceptibility to multiple pathogens in these infants, and suggest that the fetal immune system is metabolically programmed to avoid energetically costly, dispensable and potentially harmful immune responses during ontogeny.
Leukemia 2018 MAR

The T-cell leukemia-associated ribosomal RPL10 R98S mutation enhances JAK-STAT signaling.

T. Girardi et al.


Several somatic ribosome defects have recently been discovered in cancer, yet their oncogenic mechanisms remain poorly understood. Here we investigated the pathogenic role of the recurrent R98S mutation in ribosomal protein L10 (RPL10 R98S) found in T-cell acute lymphoblastic leukemia (T-ALL). The JAK-STAT signaling pathway is a critical controller of cellular proliferation and survival. A proteome screen revealed overexpression of several Jak-Stat signaling proteins in engineered RPL10 R98S mouse lymphoid cells, which we confirmed in hematopoietic cells from transgenic Rpl10 R98S mice and T-ALL xenograft samples. RPL10 R98S expressing cells displayed JAK-STAT pathway hyper-activation upon cytokine stimulation, as well as increased sensitivity to clinically used JAK-STAT inhibitors like pimozide. A mutually exclusive mutation pattern between RPL10 R98S and JAK-STAT mutations in T-ALL patients further suggests that RPL10 R98S functionally mimics JAK-STAT activation. Mechanistically, besides transcriptional changes, RPL10 R98S caused reduction of apparent programmed ribosomal frameshifting at several ribosomal frameshift signals in mouse and human Jak-Stat genes, as well as decreased Jak1 degradation. Of further medical interest, RPL10 R98S cells showed reduced proteasome activity and enhanced sensitivity to clinical proteasome inhibitors. Collectively, we describe modulation of the JAK-STAT cascade as a novel cancer-promoting activity of a ribosomal mutation, and expand the relevance of this cascade in leukemia.
The Journal of clinical investigation 2018 JUN

Dose intensification of TRAIL-inducing ONC201 inhibits metastasis and promotes intratumoral NK cell recruitment.

J. Wagner et al.


ONC201 is a first-in-class, orally active antitumor agent that upregulates cytotoxic TRAIL pathway signaling in cancer cells. ONC201 has demonstrated safety and preliminary efficacy in a first-in-human trial in which patients were dosed every 3 weeks. We hypothesized that dose intensification of ONC201 may impact antitumor efficacy. We discovered that ONC201 exerts dose- and schedule-dependent effects on tumor progression and cell death signaling in vivo. With dose intensification, we note a potent anti-metastasis effect and inhibition of cancer cell migration and invasion. Our preclinical results prompted a change in ONC201 dosing in all open clinical trials. We observed accumulation of activated NK+ and CD3+ cells within ONC201-treated tumors and that NK cell depletion inhibits ONC201 efficacy in vivo, including against TRAIL/ONC201-resistant Bax-/- tumors. Immunocompetent NCR1-GFP mice, in which NK cells express GFP, demonstrated GFP+ NK cell infiltration of syngeneic MC38 colorectal tumors. Activation of primary human NK cells and increased degranulation occurred in response to ONC201. Coculture experiments identified a role for TRAIL in human NK-mediated antitumor cytotoxicity. Preclinical results indicate the potential utility for ONC201 plus anti-PD-1 therapy. We observed an increase in activated TRAIL-secreting NK cells in the peripheral blood of patients after ONC201 treatment. The results offer what we believe to be a unique pathway of immune stimulation for cancer therapy.