EasySep™ Mouse Monocyte Isolation Kit

15-Minute cell isolation kit using immunomagnetic negative selection

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From: 688 USD


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15-Minute cell isolation kit using immunomagnetic negative selection
From: 688 USD

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The EasySep™ Mouse Monocyte Isolation Kit targets non-monocyte cells by labeling unwanted cells with antibodies and magnetic particles, and separates cells without columns using an EasySep™ magnet. Desired cells are simply poured off into a new tube. Isolated cells are immediately available for downstream applications such as flow cytometry, culture or cell-based assays.

This product replaces the EasySep™ Mouse Monocyte Enrichment Kit (Catalog #19761) for even faster cell isolations.
• Fast and easy-to-use
• Up to 95% purity
• No columns required
• Untouched, viable cells
  • EasySep™ Mouse Monocyte Isolation Kit (Catalog #19861)
    • EasySep™ Mouse Monocyte Isolation Cocktail Component A, 0.5 mL
    • EasySep™ Mouse Monocyte Isolation Cocktail Component B, 0.5 mL
    • EasySep™ Dextran RapidSpheres™ 50103, 1 mL
    • Normal Rat Serum, 2 mL
    • RoboSep™ Empty Vial
  • RoboSep™ Mouse Monocyte Isolation Kit (Catalog #19861RF)
    • EasySep™ Mouse Monocyte Isolation Cocktail Component A, 0.5 mL
    • EasySep™ Mouse Monocyte Isolation Cocktail Component B, 0.5 mL
    • EasySep™ Dextran RapidSpheres™ 50103, 1 mL
    • Normal Rat Serum, 2 mL
    • RoboSep™ Empty Vial
    • RoboSep™ Buffer (Catalog #20104)
    • RoboSep™ Filter Tips (Catalog #20125)
Magnet Compatibility:
• EasySep™ Magnet (Catalog #18000)
• “The Big Easy” EasySep™ Magnet (Catalog #18001)
• EasyEights™ EasySep™ Magnet (Catalog #18103)
• EasyPlate™ EasySep™ Magnet (Catalog #18102)
• RoboSep™-S (Catalog #21000)
Cell Isolation Kits
Cell Type:
Sample Source:
Bone Marrow; Spleen; Whole Blood
Selection Method:
Cell Isolation
Area of Interest:

Scientific Resources

Educational Materials


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


Typical EasySep™ Mouse Monocyte Isolation Profile

Figure 1. Typical EasySep™ Mouse Monocyte Isolation Profile

Starting with bone marrow cells, the monocyte content (CD11b+/CD3e-/CD45R-/CD117-/Ly-6G-/NK1.1-/Siglec F-/SSC low) of the isolated fraction is typically 94.2 ± 1.5% (mean ± SD using the purple EasySep™ Magnet).


Scientific reports 2018 OCT

Lipopolysaccharide shock reveals the immune function of indoleamine 2,3-dioxygenase 2 through the regulation of IL-6/stat3 signalling.

Y. Yamamoto et al.


Indoleamine 2,3-dioxygenase 2 (Ido2) is a recently identified catalytic enzyme in the tryptophan-kynurenine pathway that is expressed primarily in monocytes and dendritic cells. To elucidate the biological role of Ido2 in immune function, we introduced lipopolysaccharide (LPS) endotoxin shock to Ido2 knockout (Ido2 KO) mice, which led to higher mortality than that in the wild type (WT) mice. LPS-treated Ido2 KO mice had increased production of inflammatory cytokines (including interleukin-6; IL-6) in serum and signal transducer and activator of transcription 3 (stat3) phosphorylation in the spleen. Moreover, the peritoneal macrophages of LPS-treated Ido2 KO mice produced more cytokines than did the WT mice. By contrast, the overexpression of Ido2 in the murine macrophage cell line (RAW) suppressed cytokine production and decreased stat3 expression. Finally, RAW cells overexpressing Ido2 did not alter nuclear factor $\kappa$B (NF-$\kappa$B) or stat1 expression, but IL-6 and stat3 expression decreased relative to the control cell line. These results reveal that Ido2 modulates IL-6/stat3 signalling and is induced by LPS, providing novel options for the treatment of immune disorders.
The Journal of experimental medicine 2018 JAN

Sequential BMP7/TGF-β1 signaling and microbiota instruct mucosal Langerhans cell differentiation.

Capucha T et al.


Mucosal Langerhans cells (LCs) originate from pre-dendritic cells and monocytes. However, the mechanisms involved in their in situ development remain unclear. Here, we demonstrate that the differentiation of murine mucosal LCs is a two-step process. In the lamina propria, signaling via BMP7-ALK3 promotes translocation of LC precursors to the epithelium. Within the epithelium, TGF-β1 finalizes LC differentiation, and ALK5 is crucial to this process. Moreover, the local microbiota has a major impact on the development of mucosal LCs, whereas LCs in turn maintain mucosal homeostasis and prevent tissue destruction. These results reveal the differential and sequential role of TGF-β1 and BMP7 in LC differentiation and highlight the intimate interplay of LCs with the microbiota.
JCI insight 2017 SEP

Endothelium-derived extracellular vesicles promote splenic monocyte mobilization in myocardial infarction.

Akbar N et al.


Transcriptionally activated monocytes are recruited to the heart after acute myocardial infarction (AMI). After AMI in mice and humans, the number of extracellular vesicles (EVs) increased acutely. In humans, EV number correlated closely with the extent of myocardial injury. We hypothesized that EVs mediate splenic monocyte mobilization and program transcription following AMI. Some plasma EVs bear endothelial cell (EC) integrins, and both proinflammatory stimulation of ECs and AMI significantly increased VCAM-1-positive EV release. Injected EC-EVs localized to the spleen and interacted with, and mobilized, splenic monocytes in otherwise naive, healthy animals. Analysis of human plasma EV-associated miRNA showed 12 markedly enriched miRNAs after AMI; functional enrichment analyses identified 1,869 putative mRNA targets, which regulate relevant cellular functions (e.g., proliferation and cell movement). Furthermore, gene ontology termed positive chemotaxis as the most enriched pathway for the miRNA-mRNA targets. Among the identified EV miRNAs, EC-associated miRNA-126-3p and -5p were highly regulated after AMI. miRNA-126-3p and -5p regulate cell adhesion- and chemotaxis-associated genes, including the negative regulator of cell motility, plexin-B2. EC-EV exposure significantly downregulated plexin-B2 mRNA in monocytes and upregulated motility integrin ITGB2. These findings identify EVs as a possible novel signaling pathway by linking ischemic myocardium with monocyte mobilization and transcriptional activation following AMI.
Nature medicine 2016 JUL

Activation of the reward system boosts innate and adaptive immunity.

Ben-Shaanan TL et al.


Positive expectations contribute to the clinical benefits of the placebo effect. Such positive expectations are mediated by the brain's reward system; however, it remains unknown whether and how reward system activation affects the body's physiology and, specifically, immunity. Here we show that activation of the ventral tegmental area (VTA), a key component of the reward system, strengthens immunological host defense. We used 'designer receptors exclusively activated by designer drugs' (DREADDs) to directly activate dopaminergic neurons in the mouse VTA and characterized the subsequent immune response after exposure to bacteria (Escherichia coli), using time-of-flight mass cytometry (CyTOF) and functional assays. We found an increase in innate and adaptive immune responses that were manifested by enhanced antibacterial activity of monocytes and macrophages, reduced in vivo bacterial load and a heightened T cell response in the mouse model of delayed-type hypersensitivity. By chemically ablating the sympathetic nervous system (SNS), we showed that the reward system's effects on immunity are, at least partly, mediated by the SNS. Thus, our findings establish a causal relationship between the activity of the VTA and the immune response to bacterial infection.
The Journal of experimental medicine 2016 AUG

GPR91 senses extracellular succinate released from inflammatory macrophages and exacerbates rheumatoid arthritis.

Littlewood-Evans A et al.


When SUCNR1/GPR91-expressing macrophages are activated by inflammatory signals, they change their metabolism and accumulate succinate. In this study, we show that during this activation, macrophages release succinate into the extracellular milieu. They simultaneously up-regulate GPR91, which functions as an autocrine and paracrine sensor for extracellular succinate to enhance IL-1β production. GPR91-deficient mice lack this metabolic sensor and show reduced macrophage activation and production of IL-1β during antigen-induced arthritis. Succinate is abundant in synovial fluids from rheumatoid arthritis (RA) patients, and these fluids elicit IL-1β release from macrophages in a GPR91-dependent manner. Together, we reveal a GPR91/succinate-dependent feed-forward loop of macrophage activation and propose GPR91 antagonists as novel therapeutic principles to treat RA.