产品号 #19875_C
免疫磁阴性选择16分钟细胞分离
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
Products for Your Protocol
To see all required products for your protocol, please consult the Protocols and Documentation.
-
EasySep™ BufferCell separation buffer
概述
本品旨在通过负选择从小鼠组织单细胞悬液中富集1、2、3组先天淋巴样细胞（ILC1、ILC2和ilc3）。不需要的细胞是针对非ilcs和链亲和素包被磁颗粒（RapidSpheres™）的生物素化抗体靶向去除的。使用EasySep™磁铁分离标记细胞，不使用色谱柱。不需要的细胞留在管中，而需要的细胞只是被倒进一个新的管中。分离的细胞可立即用于下游应用，如流式细胞术和细胞分选。
Magnet Compatibility
• EasySep™ Magnet (Catalog #18000)
• EasyEights™ EasySep™ Magnet (Catalog #18103)
• EasyPlate™ (Catalog #18102)
Subtype
Cell Isolation Kits
Cell Type
Innate Lymphoid Cells
Species
Mouse
Sample Source
Bone Marrow, Lung, Other
Selection Method
Negative
Application
Cell Isolation
Brand
EasySep
Area of Interest
Immunology
Subtype
Cell Isolation Kits
Cell Type
Innate Lymphoid Cells
Species
Mouse
Sample Source
Bone Marrow, Lung, Other
Selection Method
Negative
Application
Cell Isolation
Brand
EasySep
Area of Interest
Immunology
Data Figures
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 (8)
Publications (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
| Species | Mouse |
|---|---|
| Magnet Compatibility | • EasySep™ Magnet (Catalog #18000) • EasyEights™ EasySep™ Magnet (Catalog #18103) • EasyPlate™ (Catalog #18102) |
| Sample Source | 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DMEM中10倍胶原酶/透明质酸酶
-
EasySep™人泛ilc富集试剂盒免疫磁阴性选择细胞富集试剂盒
标记抗体
-
抗小鼠CD3e抗体，克隆145-2C11亚美尼亚仓鼠抗小鼠CD3e单克隆IgG1抗体
-
抗小鼠Gr-1抗体，克隆RB6-8C5抗小鼠Gr-1 （Ly-6G/Ly-6C）大鼠单克隆IgG2b抗体
-
抗小鼠TCR γ / δ抗体，克隆GL3亚美尼亚仓鼠抗小鼠T细胞受体γ / δ单克隆IgG2抗体
-
抗小鼠CD19抗体，克隆1D3抗小鼠CD19的大鼠单克隆IgG2a抗体
-
抗小鼠CD45抗体，克隆30-F11抗小鼠CD45大鼠单克隆IgG2b抗体
-
抗小鼠NK1.1 （CD161）抗体，克隆PK136（C3H x BALB/c） F1杂交单克隆抗小鼠NK1.1 （CD161）抗体
-
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
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 STEMCELL, REFER TO WWW.STEMCELL.COM/COMPLIANCE.
