EasySep™ Mouse Monocyte Isolation Kit

15-Minute cell isolation kit using immunomagnetic negative selection

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From: 709 USD


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15-Minute cell isolation kit using immunomagnetic negative selection
From: 709 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

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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
EasySep; RoboSep
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).


Cell reports 2020 may

Targeting Lymph Node Niches Enhances Type 1 Immune Responses to Immunization.

J. Lian et al.


Generating robust CD4+ T-helper cell type 1 (Th1) responses is essential for protective vaccine-induced type 1 immunity. Here, we examine whether immunization formulation associated with enhanced vaccine efficacy promotes antigen targeting and cell recruitment into lymph node (LN) niches associated with optimal type 1 responses. Immunization with antigen and Toll-like receptor agonist emulsified in oil leads to an increased differentiation of IFN$\gamma$/TNF-$\alpha$+ polyfunctional Th1 cells compared to an identical immunization in saline. Oil immunization results in a rapid delivery and persistence of antigen in interfollicular regions (IFRs) of the LN, whereas without oil, antigen is distributed in the medullary region. Following oil immunization, CXCL10-producing inflammatory monocytes accumulate in the IFR, which mobilizes antigen-specific CD4+ T cells into this niche. In this microenvironment, CD4+ T cells are advantageously positioned to encounter arriving IL-12-producing inflammatory dendritic cells (DCs). These data suggest that formulations delivering antigen to the LN IFR create an inflammatory niche that can improve vaccine efficacy.
Scientific reports 2020 apr

Distinct inactivated bacterial-based immune modulators vary in their therapeutic efficacies for treating disease based on the organ site of pathology.

S. Kalyan et al.


Recent developments in understanding how the functional phenotype of the innate immune system is programmed has led to paradigm-shifting views on immunomodulation. These advances have overturned two long-held dogmas: (1) only adaptive immunity confers immunological memory; and, (2) innate immunity lacks specificity. This work describes the observation that innate immune effector cells appear to be differentially recruited to specific pathological sites when mobilized by distinct inactivated bacterial-based stimuli administered subcutaneously. The studies presented suggest that the immune system, upon detecting the first signs of a potential infection by a specific pathogen, tends to direct its resources to the compartment from which that pathogen is most likely originating. The findings from this work puts forth the novel hypothesis that the immunotherapeutic efficacy of a microbial-based stimulus for innate immune mobilization depends on the correct selection of the microbial species used as the stimulant and its relationship to the organ in which the pathology is present.
Cell host {\&} microbe 2020

TMEM173 Drives Lethal Coagulation in Sepsis.

H. Zhang et al.


The discovery of TMEM173/STING-dependent innate immunity has recently provided guidance for the prevention and management of inflammatory disorders. Here, we show that myeloid TMEM173 occupies an essential role in regulating coagulation in bacterial infections through a mechanism independent of type I interferon response. Mechanistically, TMEM173 binding to ITPR1 controls calcium release from the endoplasmic reticulum in macrophages and monocytes. The TMEM173-dependent increase in cytosolic calcium drives Gasdermin D (GSDMD) cleavage and activation, which triggers the release of F3, the key initiator of blood coagulation. Genetic or pharmacological inhibition of the TMEM173-GSDMD-F3 pathway blocks systemic coagulation and improves animal survival in three models of sepsis (cecal ligation and puncture or bacteremia with Escherichia coli or Streptococcus pneumoniae infection). The upregulation of the TMEM173 pathway correlates with the severity of disseminated intravascular coagulation and mortality in patients with sepsis. Thus, TMEM173 is a key regulator of blood clotting during lethal bacterial infections.
Scientific reports 2019 jun

Infiltrating CCR2+ monocytes and their progenies, fibrocytes, contribute to colon fibrosis by inhibiting collagen degradation through the production of TIMP-1.

N. Kuroda et al.


Intestinal fibrosis is a serious complication in inflammatory bowel disease (IBD). Despite the remarkable success of recent anti-inflammatory therapies for IBD, incidence of intestinal fibrosis and need for bowel resection have not significantly changed. To clarify the contribution of haematopoietic-derived cells in intestinal fibrosis, we prepared bone marrow (BM) chimeric mice (chimeras), which were reconstituted with BM cells derived from enhanced green fluorescent protein (EGFP)-transgenic mice or CC chemokine receptor 2 (CCR2)-deficient mice. After 2 months of transplantation, BM chimeras were treated with azoxymethane/dextran sodium sulphate. During chronic inflammation, CCR2+ BM-derived monocyte and fibrocyte infiltration into the colon and CC chemokine ligand 2 production increased, leading to colon fibrosis in EGFP BM chimeras. In CCR2-deficient BM chimeras, monocyte and fibrocyte numbers in the colonic lamina propria significantly decreased, and colon fibrosis was attenuated. In colon tissue, mRNA expression of tissue inhibitor of metalloproteinase (TIMP)-1 but not of collagen I, transforming growth factor-beta1 or matrix metalloproteinases was significantly different between the two chimeras. CCR2+ monocytes and fibrocytes showed high Timp1 mRNA expression. Our results suggest that infiltrating CCR2+ monocytes and their progenies, fibrocytes, promote colon fibrosis by inhibiting collagen degradation through TIMP-1 production.
Molecular metabolism 2019

CX3CL1-Fc treatment prevents atherosclerosis in Ldlr KO mice.

M. Riopel et al.


OBJECTIVE Atherosclerosis is a major cause of cardiovascular disease. Monocyte-endothelial cell interactions are partly mediated by expression of monocyte CX3CR1 and endothelial cell fractalkine (CX3CL1). Interrupting the interaction between this ligand-receptor pair should reduce monocyte binding to the endothelial wall and reduce atherosclerosis. We sought to reduce atherosclerosis by preventing monocyte-endothelial cell interactions through use of a long-acting CX3CR1 agonist. METHODS In this study, the chemokine domain of CX3CL1 was fused to the mouse Fc region to generate a long-acting soluble form of CX3CL1 suitable for chronic studies. CX3CL1-Fc or saline was injected twice a week (30 mg/kg) for 4 months into Ldlr knockout (KO) mice on an atherogenic western diet. RESULTS CX3CL1-Fc-treated Ldlr KO mice showed decreased en face aortic lesion surface area and reduced aortic root lesion size with decreased necrotic core area. Flow cytometry analyses of CX3CL1-Fc-treated aortic wall cell digests revealed a decrease in M1-like polarized macrophages and T cells. Moreover, CX3CL1-Fc administration reduced diet-induced atherosclerosis after switching from an atherogenic to a normal chow diet. In vitro monocyte adhesion studies revealed that CX3CL1-Fc treatment caused fewer monocytes to adhere to a human umbilical vein endothelial cell monolayer. Furthermore, a dorsal window chamber model demonstrated that CX3CL1-Fc treatment decreased in vivo leukocyte adhesion and rolling in live capillaries after short-term ischemia-reperfusion. CONCLUSION These results indicate that CX3CL1-Fc can inhibit monocyte/endothelial cell adhesion as well as reduce atherosclerosis.