Isolate highly purified human CD33+ myeloid cells from fresh human whole blood or buffy coat samples by immunomagnetic positive selection, with the EasySep™ HLA Chimerism Whole Blood CD33 Positive Selection 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™ positive selection procedure, desired cells are labeled with antibody complexes recognizing CD33 and magnetic particles. Labeled cells are separated using an EasySep™ magnet and by simply pouring or pipetting off the unwanted cells. The cells of interest remain in the tube. Following magnetic cell isolation, the desired CD33+ cells are ready for downstream applications such as flow cytometry, culture, or DNA/RNA extraction for lineage-specific chimerism analysis. The CD33 antigen is expressed on myeloid progenitor cells, granulocytes, and monocytes.
This product replaces the EasySep™ Human Whole Blood CD33 Positive Selection Kit (Catalog #18287) and EasySep™ HLA Whole Blood CD33 Positive Selection Kit (Catalog #18287HLA) for even faster cell isolations.
Learn more about how immunomagnetic EasySep™ technology works or how to fully automate immunomagnetic cell isolation with RoboSep™ to save time and increase laboratory throughput. Explore additional products optimized for your workflow, including those for cell characterization, cryopreservation, and more.
Starting with fresh whole blood, the CD33+ cell content of the isolated fraction is typically 96 ± 2% (mean ± SD) using “The Big Easy” EasySep™ Magnet. In the above example, the purities of the start (as assessed by labeling with anti-CD33) and the final isolated fractions are 68.0% and 96.2% (as assessed by labeling with anti-CD14 and anti-CD66b), respectively. NOTE: RBCs were removed from the start sample by lysis prior to flow cytometry.
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.
Antibody-Mediated LILRB2-Receptor Antagonism Induces Human Myeloid-Derived Suppressor Cells to Kill Mycobacterium tuberculosis. V. K. Singh et al. Frontiers in immunology 2022
Abstract
Tuberculosis is a leading cause of death in mankind due to infectious agents, and Mycobacterium tuberculosis (Mtb) infects and survives in macrophages (MФs). Although MФs are a major niche, myeloid-derived suppressor cells (MDSCs) are an alternative site for pathogen persistence. Both MФs and MDSCs express varying levels of leukocyte immunoglobulin-like receptor B (LILRB), which regulate the myeloid cell suppressive function. Herein, we demonstrate that antagonism of LILRB2 by a monoclonal antibody (mab) induced a switch of human MDSCs towards an M1-macrophage phenotype, increasing the killing of intracellular Mtb. Mab-mediated antagonism of LILRB2 alone and its combination with a pharmacological blockade of SHP1/2 phosphatase increased proinflammatory cytokine responses and phosphorylation of ERK1/2, p38 MAPK, and NF-kB in Mtb-infected MDSCs. LILRB2 antagonism also upregulated anti-mycobacterial iNOS gene expression and an increase in both nitric oxide and reactive oxygen species synthesis. Because genes associated with the anti-mycobacterial function of M1-MФs were enhanced in MDSCs following mab treatment, we propose that LILRB2 antagonism reprograms MDSCs from an immunosuppressive state towards a pro-inflammatory phenotype that kills Mtb. LILRB2 is therefore a novel therapeutic target for eradicating Mtb in MDSCs.
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