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Easily and efficiently isolate highly purified Group 1, 2, and 3 Innate Lymphoid Cells (ILC1, 2, and 3) from washed leukapheresis samples by immunomagnetic negative selection, with the EasySep? Human Pan-ILC Enrichment Kit. Widely used in published research for more than 20 years, EasySep? combines the specificity of monoclonal antibodies with the simplicity of a column-free magnetic system.
In this EasySep? negative selection procedure, unwanted cells are labeled with antibody complexes and magnetic particles. Unwanted cells expressing the following markers are targeted for removal: CD3, CD4, CD11c, CD14, CD16, CD19, CD24, CD34, CD36, CD61, CD66b, CD94, CD123, and GlyA. The magnetically labeled cells are then separated from the untouched desired ILCs by using an EasySep? magnet and simply pouring or pipetting the desired cells into a new tube. Following magnetic cell isolation, the desired cells are ready for downstream applications such as flow cytometry and cell sorting.
Learn more about how immunomagnetic EasySep? technology works or how to fully automate immunomagnetic cell isolation with RoboSep?. Explore additional products optimized for your workflow, including culture media, supplements, antibodies, and more.
Figure 1. Typical EasySep? Human Pan-ILC Enrichment Profile
Starting with fresh leukapheresis samples, the total ILC content (Lin-CD45+CD127+) of the enriched fraction typically ranges from 17 - 85%. In the above example, the percentages of ILCs in the start and final enriched fractions are 0.09% and 45% (or 0.1% and 54% of CD45+ cells), respectively.
This product is designed for use in the following research area(s) as part
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Single cell multi-omic analysis identifies key genes differentially expressed in innate lymphoid cells from COVID-19 patients
Frontiers in Immunology 2024 Jul
Abstract
IntroductionInnate lymphoid cells (ILCs) are enriched at mucosal surfaces where they respond rapidly to environmental stimuli and contribute to both tissue inflammation and healing. MethodsTo gain insight into the role of ILCs in the pathology and recovery from COVID-19 infection, we employed a multi-omics approach consisting of Abseq and targeted mRNA sequencing to respectively probe the surface marker expression, transcriptional profile and heterogeneity of ILCs in peripheral blood of patients with COVID-19 compared with healthy controls. ResultsWe found that the frequency of ILC1 and ILC2 cells was significantly increased in COVID-19 patients. Moreover, all ILC subsets displayed a significantly higher frequency of CD69-expressing cells, indicating a heightened state of activation. ILC2s from COVID-19 patients had the highest number of significantly differentially expressed (DE) genes. The most notable genes DE in COVID-19 vs healthy participants included a) genes associated with responses to virus infections and b) genes that support ILC self-proliferation, activation and homeostasis. In addition, differential gene regulatory network analysis revealed ILC-specific regulons and their interactions driving the differential gene expression in each ILC. DiscussionOverall, this study provides mechanistic insights into the characteristics of ILC subsets activated during COVID-19 infection.
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.
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
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