EasySep™小鼠Pan-ILC富集试剂盒

对来源于小鼠肺、淋巴结或其他组织单细胞悬液中的未标记 ILC1、ILC2 和 ILC3 细胞进行免疫磁珠负选分离

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产品号 #（选择产品）

产品号 #19875_C

16分钟免疫磁珠负选试剂盒

产品优势

操作简单、快捷，且无需分离柱
分选得到的细胞不带标记
加速ILCs的流式分选流程

产品组分包括

EasySep™小鼠Pan-ILC富集试剂盒（产品号 #19875）

EasySep™小鼠Pan-ILC富集抗体混合物，0.5 mL
EasySep™ Streptavidin RapidSpheres™ 50001磁珠，1.0 mL

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总览

使用 EasySep™ 小鼠全固有淋巴细胞富集试剂盒，可通过免疫磁性负选法从小鼠肺、淋巴结或其他组织样本的单细胞悬液中轻松高效地分离高纯度的小鼠第 1、2 和 3 类固有淋巴细胞（ILC1、ILC2 和 ILC3）。EasySep™ 技术在已发表研究中被广泛使用超过 20 年，结合了单克隆抗体的特异性与无柱磁系统的简便性。

在此 EasySep™ 负选步骤中，不需要的细胞通过抗体复合物与磁性颗粒进行标记。表达以下标志物的细胞将被去除：CD5、CD11b、CD11c、CD19、CD45R、Ly6G/C、Ter119、TCRαβ 和 TCRγδ。经 EasySep™ 磁体分离后，带有磁性标记的不需要细胞被去除，未标记的目标 ILC 细胞通过倾倒或移液方式转移至新试管中。磁性细胞分离最快可在 16 分钟内完成，目标 ILC 可直接用于流式细胞术或细胞分选等下游应用。

了解更多关于 EasySep™ 免疫磁性技术的工作原理。探索更多优化实验流程的产品，包括培养基、补充物、抗体等。

实验数据

Figure 1. Typical EasySep™ Mouse Pan-ILC Enrichment Profile

Starting with a naïve mouse lung single-cell suspension, the total ILC content (CD45+Lin-CD127+) of the enriched fraction typically ranges from 3.1 - 7.6%. In the above example, the percentages of ILCs in the start and final enriched fractions are 0.4% and 3.9% (or 0.4% and 6.8% of CD45+ cells), respectively. NOTE: The ILC content of the start fraction typically ranges from 0.3 - 0.6%.

Figure 2. Typical EasySep™ Mouse Pan-ILC Enrichment Profile from Mouse Lymph Node

Starting with a naïve mouse lymph node single-cell suspension, the total ILC content (CD45+Lin-CD127+) of the enriched fraction typically ranges from 21.1 - 45.2%. In the above example, the percentages of ILCs in the start and final enriched fractions are 0.3% and 17.6% (or 0.3% and 24.7% of CD45+ cells), respectively. NOTE: The ILC content of the start fraction typically ranges from 0.3 - 0.4%.

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。

技术资料 (8)

Mesenchymal Stem Cells Attenuate Asthmatic Inflammation and Airway Remodeling by Modulating Macrophages/Monocytes in the IL-13-Overexpressing Mouse Model. Y. Mo et al. Immune network 2022 oct

Abstract

Mesenchymal stem cells (MSCs) are attractive alternatives to conventional anti-asthmatic drugs for severe asthma. Mechanisms underlying the anti-asthmatic effects of MSCs have not yet been elucidated. This study evaluated the anti-asthmatic effects of intravenously administered MSCs, focusing on macrophages and monocytes. Seven-week-old transgenic (Tg) mice with lung-specific overexpression of IL-13 were used to simulate chronic asthma. MSCs were intravenously administered four days before sampling. We examined changes in immune cell subpopulations, gene expression, and histological phenotypes. IL-13 Tg mice exhibited diverse features of chronic asthma, including severe type 2 inflammation, airway fibrosis, and mucus metaplasia. Intravenous administration of MSCs attenuated these asthmatic features just four days after a single treatment. MSC treatment significantly reduced SiglecF-CD11c-CD11b+ monocyte-derived macrophages (MoMs) and inhibited the polarization of MoMs into M2 macrophages, especially M2a and M2c. Furthermore, MSCs downregulated the excessive accumulation of Ly6c- monocytes in the lungs. While an intravenous adoptive transfer of Ly6c- monocytes promoted the infiltration of MoM and Th2 inflammation, that of MSC-exposed Ly6c- monocytes did not. Ex vivo Ly6c- MoMs upregulated M2-related genes, which were reduced by MSC treatment. Molecules secreted by Ly6c- MoMs from IL-13 Tg mice lungs upregulated the expression of fibrosis-related genes in fibroblasts, which were also suppressed by MSC treatment. In conclusion, intravenously administered MSCs attenuate asthma phenotypes of chronic asthma by modulating macrophages. Identifying M2 macrophage subtypes revealed that exposure to MSCs transforms the phenotype and function of macrophages. We suggest that Ly6c- monocytes could be a therapeutic target for asthma management.

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OASL1-Mediated Inhibition of Type I IFN Reduces Influenza A Infection-Induced Airway Inflammation by Regulating ILC2s. Y. Chang et al. Allergy, asthma & immunology research 2022 jan

Abstract

PURPOSE Three observations drove this study. First, 2'-5'-oligoadenylate synthetase-like protein (OASL) is a negative regulator of type I interferon (IFN). Second, type I IFN plays a central role during virus infections and the pathogenesis of various diseases, including asthma. Third, influenza A virus (IAV) causes non-eosinophilic asthma. To evaluate the potential relationships between OASL, type I IFN, and pulmonary innate immune cells in IAV-induced acute airway inflammation by using Oasl1-/- mice. METHODS Asthma was induced in wild-type (WT) and Oasl1-/- mice with IAV or ovalbumin (OVA). Airway hyperreactivity (AHR) and immune cell infiltration in the bronchoalveolar lavage (BAL) fluids were measured. The immune cells in the lungs were analyzed by flow cytometry. To investigate the ability of type I IFN to shape the response of lung type 2 innate lymphoid cells (ILC2s), IFN-$\alpha$ was treated intratracheally. Plasmacytoid dendritic cells (pDCs) sorted from bone marrow and ILC2s sorted from lungs of naive mice were co-cultured with/without interferon-alpha receptor subunit 1 (IFNAR-1)-blocking antibodies. RESULTS In the IAV-induced asthma model, Oasl1-/- mice developed greater AHR and immune cell infiltration in the BAL fluids than WT mice. This was not observed in OVA-induced asthma, a standard model of allergen-induced asthma. The lungs of infected Oasl1-/- mice also had elevated DC numbers and Ifna expression and depressed IAV-induced ILC2 responses, namely, proliferation and type 2 cytokine and amphiregulin production. Intratracheal administration of type I IFN in na{\{i}}ve mice suppressed lung ILC2 production of type 2 cytokines and amphiregulin. Co-culture of ILC2s with pDCs showed that pDCs inhibit the function of ILC2s by secreting type I IFN. CONCLUSIONS OASL1 may impede the IAV-induced acute airway inflammation that drives AHR by inhibiting IAV-induced type I IFN production from lung DCs thereby preserving the functions of lung ILC2s including their amphiregulin production."

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Endothelin-A Receptor Antagonist Alleviates Allergic Airway Inflammation via the Inhibition of ILC2 Function. X. Zhang et al. Frontiers in immunology 2022

Abstract

Allergic airway inflammation is a universal airway disease that is driven by hyperresponsiveness to inhaled allergens. Group 2 innate lymphoid cells (ILC2s) produce copious amounts of type 2 cytokines, which lead to allergic airway inflammation. Here, we discovered that both peripheral blood of human and mouse lung ILC2s express the endothelin-A receptor (ETAR), and the expression level of ETAR was dramatically induced upon interleukin-33 (IL-33) treatment. Subsequently, both preventive and therapeutic effects of BQ123, an ETAR antagonist, on allergic airway inflammation were observed, which were associated with decreased proliferation and type 2 cytokine productions by ILC2s. Furthermore, ILC2s from BQ123 treatment were found to be functionally impaired in response to an interleukin IL-33 challenged. And BQ123 treatment also affected the phosphorylation level of the extracellular signal-regulated kinase (ERK), as well as the level of GATA binding protein 3 (GATA3) in activated ILC2s. Interestingly, after BQ123 treatment, both mouse and human ILC2s in vitro exhibited decreased function and downregulation of ERK signaling and GATA3 stability. These observations imply that ETAR is an important regulator of ILC2 function and may be involved in ILC2-driven pulmonary inflammation. Therefore, blocking ETAR may be a promising therapeutic strategy for allergic airway inflammation.

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更多信息

更多信息
物种	小鼠
Magnet Compatibility	• EasySep™ Magnet (Catalog #18000) • EasyEights™ EasySep™ Magnet (Catalog #18103) • EasyPlate™ (Catalog #18102)
样本来源	其它细胞系, 肺, 骨髓
Selection Method	Negative