EasySep™小鼠TIL（CD45）正选试剂盒
产品号 #19875_C
16分钟免疫磁珠负选试剂盒
若您需要咨询产品或有任何技术问题，请通过官方电话 400 885 9050 或邮箱 info.cn@stemcell.com 与我们联系
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
专为您的实验方案打造的产品
要查看实验方案所需的所有配套产品，请参阅《实验方案与技术文档》。
-
EasySep™ BufferCell separation buffer
总览
本产品通过负选从小鼠组织的单细胞悬液中富集第1、2、3型先天性淋巴细胞（ILC1、ILC2和ILC3）。利用针对非ILC细胞的生物素化抗体和链霉亲和素包被的磁珠（RapidSpheres™），来去除不需要的细胞。通过EasySep™磁极分离被标记的细胞，无需使用分离柱。目的细胞被轻松倾倒入新管中，非目的细胞保留在原分离管中。分选后的细胞可立即用于下游应用，例如流式细胞术和细胞分选。
磁体兼容性
• EasySep™ Magnet (Catalog #18000)
• EasyEights™ EasySep™ Magnet (Catalog #18103)
• EasyPlate™ (Catalog #18102)
亚型
细胞分选试剂盒
细胞类型
先天性淋巴细胞
种属
小鼠
样本来源
Bone Marrow，Lung，其它细胞系
筛选方法
Negative
应用
细胞分选
品牌
EasySep
研究领域
免疫
实验数据
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。
相关材料与文献
技术资料 (8)
文献 (3)
Mesenchymal Stem Cells Attenuate Asthmatic Inflammation and Airway Remodeling by Modulating Macrophages/Monocytes in the IL-13-Overexpressing Mouse Model. 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.
OASL1-Mediated Inhibition of Type I IFN Reduces Influenza A Infection-Induced Airway Inflammation by Regulating ILC2s. 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."
Endothelin-A Receptor Antagonist Alleviates Allergic Airway Inflammation via the Inhibition of ILC2 Function. 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.
更多信息
| 种属 | Mouse |
|---|---|
| Magnet Compatibility | • EasySep™ Magnet (Catalog #18000) • EasyEights™ EasySep™ Magnet (Catalog #18103) • EasyPlate™ (Catalog #18102) |
| 样本来源 | Bone Marrow, Lung, Other |
| Selection Method | Negative |
相关产品
-
氯化铵溶液红细胞裂解试剂
-
胶原酶/透明质酸酶配置于DMEM中的10 X 胶原酶/透明质酸酶
-
EasySep™人Pan-ILC富集试剂盒免疫磁珠负选细胞富集试剂盒
标记抗体
-
抗小鼠CD19抗体，克隆ID3大鼠单克隆IgG2a抗体，抗小鼠CD19
-
抗小鼠CD3e抗体，克隆145-2C11亚美尼亚仓鼠单克隆IgG1抗体，抗小鼠CD3e
-
抗小鼠CD45抗体，克隆30-F11大鼠单克隆IgG2b抗体，抗小鼠CD45
-
抗小鼠Gr-1抗体，克隆RB6-8C5大鼠单克隆IgG2b抗体，抗小鼠Gr-1 （Ly-6G/Ly-6C）
-
抗小鼠NK1.1（CD161）抗体，克隆PK136抗小鼠 NK1.1 (CD161) 的 (C3H x BALB/c) F1 杂交单克隆IgG2a抗体
-
抗小鼠TCR Gamma/Delta 抗体，克隆GL3亚美尼亚仓鼠单克隆IgG2抗体，抗小鼠T细胞受体 gamma/delta
-
抗小鼠TER119抗体，克隆TER-119抗小鼠TER119的大鼠（WI）单克隆IgG2b抗体
-
抗小鼠CD11b抗体，克隆M1/70抗人、小鼠、恒河猴CD11b的大鼠单克隆IgG2b抗体
