EasySep? Human Na?ve CD4+ T Cell Isolation Kit II
Immunomagnetic negative isolation of untouched human na?ve CD4+ T cells
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Products for Your Protocol
To see all required products for your protocol, please consult the
Protocols and Documentation.
- EasySep? Magnet
Magnet for column-free immunomagnetic separation
- EasySep? Buffer
Cell separation buffer for use with EasySep? cell separation kits
Overview
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Protocols and Documentation
Find supporting information and directions for use in the Product Information Sheet or explore additional protocols below.
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.
Resources and Publications
Educational Materials (10)
Publications (13)
LINC01871 is exclusively expressed in T and NK cells and is highly induced upon CD4+ T cell activation
iScience 2025 Oct
Abstract
SummaryLong intergenic noncoding RNAs (lincRNAs) regulate biological processes in health and disease. Recent findings highlight the importance of lincRNAs in regulating T cell development and function. Here, we identified a lincRNA, LINC01871, which is highly induced upon CD4+ T cell activation and is predominantly located in the cytoplasm. The anti-inflammatory cytokine TGF-β was found to suppress its expression. Silencing LINC01871 led to a modest decrease in IL-2 secretion. Notably, LINC01871 expression was highly specific to NK cells and T cells in several cross-tissue single cell RNA-seq atlases. These data suggest that LINC01871 is specifically expressed in T and NK cells and may contribute to T cell-mediated immunity in humans. Graphical abstract Highlights?LINC01871 is a cytoplasmic lincRNA induced upon CD4+ T cell activation?TGF-β negatively regulates LINC01871 expression?Expression of LINC01871 is restricted to effector and memory T and NK cells Immunology; Molecular biology; Cell biology
Interferon-β and interleukin-6 exert opposing effects on Foxp3 acetylation to control regulatory T cell induction.
Frontiers in immunology 2025 May
Abstract
Cytokines are key soluble signaling molecules that regulate immune responses. With the advent of therapies that selectively target cytokines and cytokine receptors, understanding the molecular mechanisms underpinning how immune cells integrate multiple cytokine signals has become a critical challenge in immunology. However, the pleiotropic nature of cytokines makes it difficult to decipher their precise contributions in various contexts. Here, we used an integrated experimental and computational approach to investigate the combined effect and interplay between the pro-inflammatory cytokine interleukin-6 (IL-6) and interferon-beta (IFNβ), also a pro-inflammatory cytokine with potent antiviral properties, in modulating regulatory T cell (Treg) induction. Our studies reveal that, in contrast with its pro-inflammatory role in innate immune responses, IFNβ can counteract the well-described inhibitory effect of IL-6 on Treg induction. Mechanistically, we demonstrate that IFNβ and IL-6 signal independently to promote opposing effects on the acetylation of Foxp3, an essential transcription factor governing Treg differentiation, stability, and function. We further show that this mechanism is conserved in both murine and human T cells, highlighting the broad relevance of this finding in immune regulation. These results have important implications for the numerous contexts in which IFNβ and IL-6 co-exist, including viral infection, transplantation, and autoimmune disease.
Single-cell ultra-high-throughput multiplexed chromatin and RNA profiling reveals gene regulatory dynamics
Nature Methods 2025 May
Abstract
Enhancers and transcription factors (TFs) are crucial in regulating cellular processes. Current multiomic technologies to study these elements in gene regulatory mechanisms lack multiplexing capability and scalability. Here we present single-cell ultra-high-throughput multiplexed sequencing (SUM-seq) for co-assaying chromatin accessibility and gene expression in single nuclei. SUM-seq enables profiling hundreds of samples at the million cell scale and outperforms current high-throughput single-cell methods. We demonstrate the capability of SUM-seq to (1) resolve temporal gene regulation of macrophage M1 and M2 polarization to bridge TF regulatory networks and immune disease genetic variants, (2) define the regulatory landscape of primary T helper cell subsets and (3) dissect the effect of perturbing lineage TFs via arrayed CRISPR screens in spontaneously differentiating human induced pluripotent stem cells. SUM-seq offers a cost-effective, scalable solution for ultra-high-throughput single-cell multiomic sequencing, accelerating the unraveling of complex gene regulatory networks in cell differentiation, responses to perturbations and disease studies. This work presents SUM-seq, an ultra-high-throughput method for co-profiling chromatin accessibility and gene expression in single nuclei across multiplexed samples, advancing the study of gene regulation in diverse biological systems.
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PRODUCTS ARE FOR RESEARCH USE ONLY AND NOT INTENDED FOR HUMAN OR ANIMAL DIAGNOSTIC OR THERAPEUTIC USES UNLESS OTHERWISE STATED. FOR ADDITIONAL INFORMATION ON QUALITY AT 海角破解版, REFER TO WWW.海角破解版.COM/COMPLIANCE.
PRODUCTS ARE FOR RESEARCH USE ONLY AND NOT INTENDED FOR HUMAN OR ANIMAL DIAGNOSTIC OR THERAPEUTIC USES UNLESS OTHERWISE STATED. FOR ADDITIONAL INFORMATION ON QUALITY AT 海角破解版, REFER TO WWW.海角破解版.COM/COMPLIANCE.
