The EasySep™ Human Pan-ILC Enrichment Kit is designed to enrich Group 1, 2, and 3 Innate Lymphoid Cells (ILC1, 2, and 3) from leukapheresis products by immunomagnetic negative selection. Unwanted cells are targeted for removal by Tetrameric Antibody Complexes directed against non-ILCs and dextran-coated magnetic particles (RapidSpheres™). Labeled cells are separated using an EasySep™ magnet without the use of columns. Unwanted cells remain in the tube as enriched ILCs are simply poured off into a new tube. Isolated cells are immediately available for flow sorting and other downstream applications.
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 of the highlighted workflow stage(s). Explore these workflows to learn more about the other products we offer to support each research area.
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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