EasySep™人初始CD4+ T细胞分选试剂盒II

免疫磁珠负选获取未被标记的人初始 CD4+ T 细胞

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产品号 #（选择产品）

产品号 #17555_C

免疫磁珠负选分选法获取未被标记的人初始CD4+ T细胞

产品优势

操作简单、快捷，且无需分离柱
纯度可高达98%
获得无磁珠标记的活性细胞

产品组分包括

EasySep™人Naïve CD4+ T细胞分选试剂盒 II（产品号 #17555）
- EasySep™人Naïve CD4+ T细胞分选抗体混合物II，1mL
- EasySep™ Dextran RapidSpheres™磁珠，1mL
RoboSep™ 人Naïve CD4+ T细胞分选试剂盒II（产品号 #17555RF）
- EasySep™人Naïve CD4+ T细胞分选抗体混合物II,1mL
- EasySep™ Dextran RapidSpheres™磁珠，1mL
- RoboSep™ 缓冲液（产品号 #20104）
- RoboSep™过滤吸头（产品号 #20125）

立即询价

总览

使用EasySep™人naïve CD4+ T细胞分选试剂盒II，通过免疫磁珠负选，即可从新鲜或冻存的人外周血单个核细胞（PBMC）样本中轻松高效地分离出高纯度的人naïve CD4+ T细胞（CD3+CD4+CD45RA+CD45RO-）。EasySep™在已发表的研究中被广泛使用了20多年，它结合了单克隆抗体的特异性和无柱磁珠系统的简便性。

在此EasySep™负选过程中，非目的细胞被抗体复合物和磁珠标记。表达以下标志物的非目的细胞将被定位并去除：CD8、CD14、CD16、CD19、CD20、CD25、CD36、CD45RO、CD56、CD61、CD66b、CD123、GlyA、TCRgd和HLA-DR。然后使用EasySep™磁极将磁珠标记的细胞与未标记的目的naïve CD4+ T细胞分离，只需将所需细胞倒入或移液到新试管中即可。磁珠分选过程仅需11分钟，获得的naïve CD4+ T细胞可立即用于下游应用，例如流式细胞术、培养或DNA/RNA提取。

该试剂盒取代了EasySep™人naïve CD4+ T细胞富集试剂盒（产品号 #19155）和EasySep™人naïve CD4+ T细胞分选试剂盒（产品号 #19555），可实现更快的细胞分选。

了解有关EasySep™免疫磁珠技术的工作原理或如何使用RoboSep™进行全自动免疫磁珠细胞分选的更多信息。此外，您还可以选择使用EasySep™人naïve CD4+ T细胞分选试剂盒II分离的即用型且来源符合伦理规范的原代冻存人外周血CD4+CD45RA+ T细胞。探索针对您的工作流程进行优化的其他产品，包括培养基、添加物、抗体等。
19555

实验数据

Figure 1. Typical EasySep™ Human Naive CD4 T Cell Isolation Profile

Starting with fresh mononuclear cells, the naïve CD4+ T cell content (CD3+CD4+CD45RA+CD45RO-) of the isolated fraction is typically 96.6 ± 1.5% (mean ± SD using the purple EasySep™ Magnet). In the above example, the purities of the start and final isolated fractions are 13.0% and 97.3%, respectively.

产品说明书及文档

请在《产品说明书》中查找相关支持信息和使用说明，或浏览下方更多实验方案。

文献 (7)

Soluble RAGE Prevents Type 1 Diabetes Expanding Functional Regulatory T Cells. S. S. Leung et al. Diabetes 2022 sep

Abstract

Type 1 diabetes is an autoimmune disease with no cure, where clinical translation of promising therapeutics has been hampered by the reproducibility crisis. Here, short-term administration of an antagonist to the receptor for advanced glycation end products (sRAGE) protected against murine diabetes at two independent research centers. Treatment with sRAGE increased regulatory T cells (Tregs) within the islets, pancreatic lymph nodes, and spleen, increasing islet insulin expression and function. Diabetes protection was abrogated by Treg depletion and shown to be dependent on antagonizing RAGE with use of knockout mice. Human Tregs treated with a RAGE ligand downregulated genes for suppression, migration, and Treg homeostasis (FOXP3, IL7R, TIGIT, JAK1, STAT3, STAT5b, CCR4). Loss of suppressive function was reversed by sRAGE, where Tregs increased proliferation and suppressed conventional T-cell division, confirming that sRAGE expands functional human Tregs. These results highlight sRAGE as an attractive treatment to prevent diabetes, showing efficacy and reproducibility at multiple research centers and in human T cells.

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Blocking CCL8-CCR8-Mediated Early Allograft Inflammation Improves Kidney Transplant Function. A. Dangi et al. Journal of the American Society of Nephrology : JASN 2022 oct

Abstract

BACKGROUND In kidney transplantation, early allograft inflammation impairs long-term allograft function. However, precise mediators of early kidney allograft inflammation are unclear, making it challenging to design therapeutic interventions. METHODS We used an allogeneic murine kidney transplant model in which CD45.2 BALB/c kidneys were transplanted to CD45.1 C57BL/6 recipients. RESULTS Donor kidney resident macrophages within the allograft expanded rapidly in the first 3 days. During this period, they were also induced to express a high level of Ccl8, which, in turn, promoted recipient monocyte graft infiltration, their differentiation to resident macrophages, and subsequent expression of Ccl8. Enhanced graft infiltration of recipient CCR8+ T cells followed, including CD4, CD8, and ?? T cells. Consequently, blocking CCL8-CCR8 or depleting donor kidney resident macrophages significantly inhibits early allograft immune cell infiltration and promotes superior short-term allograft function. CONCLUSIONS Targeting the CCL8-CCR8 axis is a promising measure to reduce early kidney allograft inflammation.

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Age-associated impairment of T cell immunity is linked to sex-dimorphic elevation of N-glycan branching. H. Mkhikian et al. Nature aging 2022 mar

Abstract

Impaired T cell immunity with aging increases mortality from infectious disease. The branching of Asparagine-linked glycans is a critical negative regulator of T cell immunity. Here we show that branching increases with age in females more than males, in na{\{i}}ve more than memory T cells and in CD4+ more than CD8+ T cells. Female sex hormones and thymic output of na{\"{i}}ve T cells (TN) decrease with age however neither thymectomy nor ovariectomy altered branching. Interleukin-7 (IL-7) signaling was increased in old female more than male mouse TN cells and triggered increased branching. N-acetylglucosamine a rate-limiting metabolite for branching increased with age in humans and synergized with IL-7 to raise branching. Reversing elevated branching rejuvenated T cell function and reduced severity of Salmonella infection in old female mice. These data suggest sex-dimorphic antagonistic pleiotropy where IL-7 initially benefits immunity through TN maintenance but inhibits TN function by raising branching synergistically with age-dependent increases in N-acetylglucosamine."

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更多信息

更多信息
物种	人类
Magnet Compatibility	• EasySep™ Magnet (Catalog #18000) • “The Big Easy” EasySep™ Magnet (Catalog #18001) • Easy 50 EasySep™ Magnet (Catalog #18002) • EasyEights™ EasySep™ Magnet (Catalog #18103) • RoboSep™-S (Catalog #21000)
样本来源	PBMC
Selection Method	Negative