EasySep™小鼠CD4+CD25+调节性T细胞分选试剂盒II

通过免疫磁珠正选分离小鼠CD4+CD25+调节性T细胞

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产品号 #（选择产品）

产品号 #18783_C

通过免疫磁珠正选分离小鼠CD4+CD25+调节性T细胞

产品优势

快速、易于操作
纯度高达93%
无需分离柱

产品组分包括

EasySep™小鼠CD4+CD25+调节性T细胞分离试剂盒II（产品号 #18783）

EasySep™小鼠CD4+ T细胞分选抗体混合物，0.5mL
EasySep™ Streptavidin RapidSpheres™ 50001磁珠，1mL
EasySep™小鼠CD25调节性T细胞正选抗体混合物，0.5mL
EasySep™PE分选抗体混合物，1mL
EasySep™ Dextran RapidSpheres™ 50100 磁珠，1mL
EasySep™小鼠FcR阻断剂（产品号 #18731），0.5mL

RoboSep™小鼠CD4+ CD25+调节性T细胞分选试剂盒II（产品号 #18783RF）

EasySep™小鼠CD4+ T细胞分选抗体混合物，0.5mL
EasySep™ Streptavidin RapidSpheres™ 50001磁珠，1mL
EasySep™小鼠CD25调节性T细胞正选抗体混合物，0.5mL
EasySep™PE分选抗体混合物，1mL
EasySep™ Dextran RapidSpheres™ 50100 磁珠，1mL
EasySep™小鼠FcR阻断剂（产品号 #18731），0.5mL
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™小鼠CD4+CD25+调节性T细胞分选试剂盒II，通过简单的两步法（首先进行免疫磁珠负选，然后使用正选），即可轻松从小鼠脾细胞或其他单细胞悬液样本中分离出高纯度的小鼠CD4+CD25+调节性T细胞（Tregs）。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™细胞分选过程中，首先使用EasySep™小鼠CD4+ T细胞分选抗体混合物通过负选富集CD4+ T细胞。然后使用EasySep™小鼠CD25调节性T细胞正选抗体混合物从预富集的细胞中正选分离出CD25+细胞。完成磁珠分选后，获得的CD4+CD25+ Tregs即可用于下游应用，例如流式细胞术、培养、DNA/RNA提取。

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。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。

实验数据

FACS Histogram Results with EasySep™ Mouse CD4+CD25+ Regulatory T Cell Isolation Kit II

Figure 1. Typical EasySep™ Mouse CD4+CD25+ Regulatory T Cell Isolation Profile

Starting with mouse splenocytes, the regulatory T cell content (CD4+CD25+FOXP3+) of the isolated fraction typically ranges from 70 - 93%. In the above example, the purities of the start and final isolated fractions are 2% and 72%, 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。

应用领域

本产品专为以下研究领域设计，适用于工作流程中的高亮阶段。探索这些工作流程，了解更多我们为各研究领域提供的其他配套产品。

常见问题 (7)

文献 (11)

PARP11 inhibition inactivates tumor-infiltrating regulatory T cells and improves the efficacy of immunotherapies Cell Reports Medicine 2024 Jul

Abstract

SummaryTumor-infiltrating regulatory T cells (TI-Tregs) elicit immunosuppressive effects in the tumor microenvironment (TME) leading to accelerated tumor growth and resistance to immunotherapies against solid tumors. Here, we demonstrate that poly-(ADP-ribose)-polymerase-11 (PARP11) is an essential regulator of immunosuppressive activities of TI-Tregs. Expression of PARP11 correlates with TI-Treg cell numbers and poor responses to immune checkpoint blockade (ICB) in human patients with cancer. Tumor-derived factors including adenosine and prostaglandin E2 induce PARP11 in TI-Tregs. Knockout of PARP11 in the cells of the TME or treatment of tumor-bearing mice with selective PARP11 inhibitor ITK7 inactivates TI-Tregs and reinvigorates anti-tumor immune responses. Accordingly, ITK7 decelerates tumor growth and significantly increases the efficacy of anti-tumor immunotherapies including ICB and adoptive transfer of chimeric antigen receptor (CAR) T cells. These results characterize PARP11 as a key driver of TI-Treg activities and a major regulator of immunosuppressive TME and argue for targeting PARP11 to augment anti-cancer immunotherapies. Graphical abstract Highlights•Tumor-derived factors upregulate PARP11 in the tumor-infiltrating Treg cells•PARP11 supports the immunosuppressive properties of Treg cells•Pharmacologic inhibition of PARP11 inactivates intratumoral Treg cells•PARP11 inhibitor augments the efficacy of immunotherapies Basavaraja et al. demonstrate that induction of PARP11 in the intratumoral regulatory T (Treg) cells is required for their regulatory functions and contributes to the immunosuppressive tumor microenvironment. The selective inhibitor of PARP11 ITK7 inactivates tumor Treg cells and improves the efficacy of immunotherapies against tumors.

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Low-dose IL-2 prevents murine chronic cardiac allograft rejection: Role for IL-2-induced T regulatory cells and exosomes with PD-L1 and CD73. R. Ravichandran et al. American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons 2022 sep

Abstract

To determine the effects and immunological mechanisms of low-dose interleukin-2 (IL-2) in a murine model of chronic cardiac allograft rejection (BALB/c to C57BL/6) after costimulatory blockade consisting of MR1 (250??$\mu$g/ip day 0) and CTLA4-Ig (200??$\mu$g/ip day 2), we administered low-dose IL-2 (2000??IU/day) starting on posttransplant day 14 for 3??weeks. T regulatory (Treg) cell infiltration of the grafts was determined by immunohistochemistry; circulating exosomes by western blot and aldehyde bead flow cytometry; antibodies to donor MHC by immunofluorescent staining of donor cells; and antibodies to cardiac self-antigens (myosin, vimentin) by ELISA. We demonstrated that costimulation blockade after allogeneic heart transplantation induced circulating exosomes containing cardiac self-antigens and antibodies to both donor MHC and self-antigens, leading to chronic rejection by day 45. Treatment with low-dose IL-2 prolonged allograft survival (>100??days), prevented chronic rejection, and induced splenic and graft-infiltrating CD4+ CD25+ Foxp3 Treg cells by day 45 and circulating exosomes (Foxp3+) with PD-L1 and CD73. MicroRNA 142, associated with the TGF$\beta$ pathway, was significantly downregulated in exosomes from IL-2-treated mice. In conclusion, low-dose IL-2 delays rejection in a murine model of chronic cardiac allograft rejection and also induces graft-infiltrating Tregs and circulating exosomes with immunoregulatory molecules.

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Blockades of effector T cell senescence and exhaustion synergistically enhance antitumor immunity and immunotherapy. X. Liu et al. Journal for immunotherapy of cancer 2022 oct

Abstract

BACKGROUND Current immunotherapies still have limited successful rates among cancers. It is now recognized that T cell functional state in the tumor microenvironment (TME) is a key determinant for effective antitumor immunity and immunotherapy. In addition to exhaustion, cellular senescence in tumor-infiltrating T cells (TILs) has recently been identified as an important T cell dysfunctional state induced by various malignant tumors. Therefore, a better understanding of the molecular mechanism responsible for T cell senescence in the TME and development of novel strategies to prevent effector T cell senescence are urgently needed for cancer immunotherapy. METHODS Senescent T cell populations in the TMEs in mouse lung cancer, breast cancer, and melanoma tumor models were evaluated. Furthermore, T cell senescence induced by mouse tumor and regulatory T (Treg) cells in vitro was determined with multiple markers and assays, including real-time PCR, flow cytometry, and histochemistry staining. Loss-of-function strategies with pharmacological inhibitors and the knockout mouse model were used to identify the potential molecules and pathways involved in T cell senescence. In addition, melanoma mouse tumor immunotherapy models were performed to explore the synergistical efficacy of antitumor immunity via prevention of tumor-specific T cell senescence combined with anti-programmed death-ligand 1 (anti-PD-L1) checkpoint blockade therapy. RESULTS We report that both mouse malignant tumor cells and Treg cells can induce responder T cell senescence, similar as shown in human Treg and tumor cells. Accumulated senescent T cells also exist in the TME in tumor models of lung cancer, breast cancer and melanoma. Induction of ataxia-telangiectasia mutated protein (ATM)-associated DNA damage is the cause for T cell senescence induced by both mouse tumor cells and Treg cells, which is also regulated by mitogen-activated protein kinase (MAPK) signaling. Furthermore, blockages of ATM-associated DNA damage and/or MAPK signaling pathways in T cells can prevent T cell senescence mediated by tumor cells and Treg cells in vitro and enhance antitumor immunity and immunotherapy in vivo in adoptive transfer T cell therapy melanoma models. Importantly, prevention of tumor-specific T cell senescence via ATM and/or MAPK signaling inhibition combined with anti-PD-L1 checkpoint blockade can synergistically enhance antitumor immunity and immunotherapy in vivo. CONCLUSIONS These studies prove the novel concept that targeting both effector T cell senescence and exhaustion is an effective strategy and can synergistically enhance cancer immunotherapy.

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物种	小鼠
Magnet Compatibility	• EasySep™ Magnet (Catalog #18000) • “The Big Easy” EasySep™ Magnet (Catalog #18001) • EasyEights™ Magnet (Catalog #18103) • RoboSep™-S (Catalog #21000)
样本来源	脾脏

EasySep™小鼠CD4+CD25+调节性T细胞分选试剂盒II

产品号 #18783

产品号 #18783RF

产品号 #（选择产品）

产品号 #18783_C

产品优势

产品组分包括

总览

实验数据

产品说明书及文档

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相关材料与文献

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Scientists Helping Scientists™

EasySep™小鼠CD4+CD25+调节性T细胞分选试剂盒II

产品号 #18783

产品号 #18783RF

产品号 #（选择产品）

产品号 #18783_C

产品优势

产品组分包括

总览

实验数据

产品说明书及文档

应用领域

相关材料与文献

技术资料 (11)

常见问题 (7)

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

How does the separation work?

Which columns do I use?

How can I analyze the purity of my enriched sample?

Can EasySep™ Streptavidin RapidSphere™ separations be automated?

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

Can I alter the separation time in the magnet?

文献 (11)

Abstract

Abstract

Abstract

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