EasySep™ Mouse Naïve CD4+ T Cell Isolation Kit

15-Minute cell isolation kit using immunomagnetic negative selection

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From: 674 USD


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15-Minute cell isolation kit using immunomagnetic negative selection
From: 674 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 Naïve CD4+ T Cell Isolation Kit is designed to isolate naïve CD4+ T cells from single-cell suspensions of splenocytes or other tissues by negative selection. Unwanted cells are targeted for removal with biotinylated antibodies directed against non-naïve CD4+ T cells (CD8, CD11b, CD11c, CD19, CD24, CD25, CD44, CD45R, CD49b, TCRγ/δ, TER119) and streptavidin-coated magnetic particles (RapidSpheres™ ). Labeled cells are separated using an EasySep™ magnet without the use of columns. Desired cells are poured off into a new tube.

Learn more about our next-generation EasySep™ mouse cell isolation kits, featuring RapidSphere™ technology.
• Fast, easy-to-use and column-free
• Up to 95% purity
• Untouched, viable cells
  • EasySep™ Mouse Naïve CD4+ T Cell Isolation Kit (Catalog #19765)
    • EasySep™ Mouse CD4+ T Cell Isolation Cocktail, 0.5 mL
    • EasySep™ Mouse Memory T Cell Depletion Cocktail, 0.5 mL
    • EasySep™ Streptavidin RapidSpheres™ 50001, 1 mL
    • Normal Rat Serum, 2 mL
  • RoboSep™ Mouse Naïve CD4+ T Cell Isolation Kit (Catalog #19765RF)
    • EasySep™ Mouse CD4+ T Cell Isolation Cocktail, 0.5 mL
    • EasySep™ Mouse Memory T Cell Depletion Cocktail, 0.5 mL
    • EasySep™ Streptavidin RapidSpheres™ 50001, 1 mL
    • Normal Rat Serum, 2 mL
    • 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)
• RoboSep™-S (Catalog #21000)
Cell Isolation Kits
Cell Type:
T Cells; T Cells, CD4+
Sample Source:
Other; Spleen
Selection Method:
Cell Isolation
EasySep; RoboSep
Area of Interest:

Scientific Resources

Educational Materials


Frequently Asked Questions

Can EasySep™ Streptavidin RapidSpheres™ be used for either positive or negative selection?

Currently, EasySep™ Streptavidin RapidSphere™ kits are only available for negative selection and work by targeting and removing unwanted cells.

How does the separation work?

Streptavidin RapidSphere™ magnetic particles are crosslinked to unwanted cells using biotinylated antibodies. When placed in the EasySep™ Magnet, labeled cells migrate to the wall of the tube. The unlabeled cells are then poured off into a new tube.

Which columns do I use?

The EasySep™ procedure is column-free. That's right - no columns!

How can I analyze the purity of my enriched sample?

The Product Information Sheet provided with each EasySep™ kit contains detailed staining information.

Can EasySep™ Streptavidin RapidSphere™ separations be automated?

Yes. RoboSep™, the fully automated cell separator, automates all EasySep™ labeling and cell separation steps.

Are cells isolated using EasySep™ RapidSphere™ products FACS-compatible?

Yes. Desired cells are unlabeled and ready to use in downstream applications, such as FACS analysis.

Can I alter the separation time in the magnet?

Yes; however, this may impact the kit's performance. The provided EasySep™ protocols have already been optimized to balance purity, recovery and time spent on the isolation.
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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


Typical EasySep™ Mouse Naïve CD4+ T Cell Isolation Profile

Figure 1. Typical EasySep™ Mouse Naïve CD4+ T Cell Isolation Profile

Starting with mouse splenocytes from an uninfected mouse, the naïve CD4+ T cell (CD4+CD44lowCD62Lhigh) content of the isolated fraction typically ranges from 89.9 - 95.6%. In the example above, the final purities of the start and isolated fractions are 14.3% and 94.7%, respectively.


Nature biomedical engineering 2020 oct

Prolonged residence of an albumin-IL-4 fusion protein in secondary lymphoid organs ameliorates experimental autoimmune encephalomyelitis.

A. Ishihara et al.


Interleukin-4 (IL-4) suppresses the development of multiple sclerosis in a murine model of experimental autoimmune encephalomyelitis (EAE). Here, we show that, in mice with EAE, the accumulation and persistence in the lymph nodes and spleen of a systemically administered serum albumin (SA)-IL-4 fusion protein leads to higher efficacy in preventing disease development than the administration of wild-type IL-4 or of the clinically approved drug fingolimod. We also show that the SA-IL-4 fusion protein prevents immune-cell infiltration in the spinal cord, decreases integrin expression in antigen-specific CD4+ T cells, increases the number of granulocyte-like myeloid-derived suppressor cells (and their expression of programmed-death-ligand-1) in spinal cord-draining lymph nodes and decreases the number of T helper 17 cells, a pathogenic cell population in EAE. In mice with chronic EAE, SA-IL-4 inhibits immune-cell infiltration into the spinal cord and completely abrogates immune responses to myelin antigen in the spleen. The SA-IL-4 fusion protein may be prophylactically and therapeutically advantageous in the treatment of multiple sclerosis.
Science advances 2020 jun

Synoviocyte-targeted therapy synergizes with TNF inhibition in arthritis reversal.

M. N. D. Svensson et al.


Fibroblast-like synoviocytes (FLS) are joint-lining cells that promote rheumatoid arthritis (RA) pathology. Current disease-modifying antirheumatic agents (DMARDs) operate through systemic immunosuppression. FLS-targeted approaches could potentially be combined with DMARDs to improve control of RA without increasing immunosuppression. Here, we assessed the potential of immunoglobulin-like domains 1 and 2 (Ig1{\&}2), a decoy protein that activates the receptor tyrosine phosphatase sigma (PTPRS) on FLS, for RA therapy. We report that PTPRS expression is enriched in synovial lining RA FLS and that Ig1{\&}2 reduces migration of RA but not osteoarthritis FLS. Administration of an Fc-fusion Ig1{\&}2 attenuated arthritis in mice without affecting innate or adaptive immunity. Furthermore, PTPRS was down-regulated in FLS by tumor necrosis factor (TNF) via a phosphatidylinositol 3-kinase-mediated pathway, and TNF inhibition enhanced PTPRS expression in arthritic joints. Combination of ineffective doses of TNF inhibitor and Fc-Ig1{\&}2 reversed arthritis in mice, providing an example of synergy between FLS-targeted and immunosuppressive DMARD therapies.
Cell reports 2020 feb

Mitochondrial Oxidative Phosphorylation Regulates the Fate Decision between Pathogenic Th17 and Regulatory T Cells.

B. Shin et al.


Understanding metabolic pathways that regulate Th17 development is important to broaden therapeutic options for Th17-mediated autoimmunity. Here, we report a pivotal role of mitochondrial oxidative phosphorylation (OXPHOS) for lineage specification toward pathogenic Th17 differentiation. Th17 cells rapidly increase mitochondrial respiration during development, and this is necessary for metabolic reprogramming following T cell activation. Surprisingly, specific inhibition of mitochondrial ATP synthase ablates Th17 pathogenicity in a mouse model of autoimmunity by preventing Th17 pathogenic signature gene expression. Notably, cells activated under OXPHOS-inhibited Th17 conditions preferentially express Foxp3, rather than Th17 genes, and become suppressive Treg cells. Mechanistically, OXPHOS promotes the Th17 pioneer transcription factor, BATF, and facilitates T cell receptor (TCR) and mTOR signaling. Correspondingly, overexpression of BATF rescues Th17 development when ATP synthase activity is restricted. Together, our data reveal a regulatory role of mitochondrial OXPHOS in dictating the fate decision between Th17 and Treg cells by supporting early molecular events necessary for Th17 commitment.
Nature communications 2020

T cell-intrinsic role for Nod2 in protection against Th17-mediated uveitis.

R. J. Napier et al.


Mutations in nucleotide-binding oligomerization domain-containing protein 2 (NOD2) cause Blau syndrome, an inflammatory disorder characterized by uveitis. The antimicrobial functions of Nod2 are well-established, yet the cellular mechanisms by which dysregulated Nod2 causes uveitis remain unknown. Here, we report a non-conventional, T cell-intrinsic function for Nod2 in suppression of Th17 immunity and experimental uveitis. Reconstitution of lymphopenic hosts with Nod2-/- CD4+ T cells or retina-specific autoreactive CD4+ T cells lacking Nod2 reveals a T cell-autonomous, Rip2-independent mechanism for Nod2 in uveitis. In naive animals, Nod2 operates downstream of TCR ligation to suppress activation of memory CD4+ T cells that associate with an autoreactive-like profile involving IL-17 and Ccr7. Interestingly, CD4+ T cells from two Blau syndrome patients show elevated IL-17 and increased CCR7. Our data define Nod2 as a T cell-intrinsic rheostat of Th17 immunity, and open new avenues for T cell-based therapies for Nod2-associated disorders such as Blau syndrome.
Scientific reports 2019 apr

Maf deficiency in T cells dysregulates Treg - TH17 balance leading to spontaneous colitis.

C. Imbratta et al.


The maintenance of homeostasis in the gut is a major challenge for the immune system. Here we demonstrate that the transcription factor MAF plays a central role in T cells for the prevention of gastro-intestinal inflammation. Conditional knock out mice lacking Maf in all T cells developed spontaneous late-onset colitis, correlating with a decrease of FOXP3+RORgammat+ T cells proportion, dampened IL-10 production in the colon and an increase of inflammatory TH17 cells. Strikingly, FOXP3+ specific conditional knock out mice for MAF did not develop colitis and demonstrated normal levels of IL-10 in their colon, despite the incapacity of regulatory T cells lacking MAF to suppress colon inflammation in Rag1-/- mice transferred with na{\{i}}ve CD4+ T cells. We showed that one of the cellular sources of IL-10 in the colon of these mice are TH17 cells. Thus MAF is critically involved in the maintenance of the gut homeostasis by regulating the balance between Treg and TH17 cells either at the level of their differentiation or through the modulation of their functions."