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Efficiently isolate or deplete human CD11b+ cells from fresh or previously frozen peripheral blood mononuclear cells (PBMCs) or leukapheresis samples in as little as 16 minutes. Cells isolated with the EasySep? Human CD11b Positive Selection and Depletion Kit can be used immediately in downstream applications such as flow cytometry, cell culture, or DNA/RNA extraction.
Use this kit to label CD11b+ cells with antibodies and magnetic particles. The cells are then subsequently separated—without the use of columns—using an EasySep? magnet. Labeled cells remain in the tube while unlabeled cells are poured off. Depending on your research needs, either fraction can be retained for subsequent applications.
This kit targets human CD11b, a subunit of the integrin macrophage-1 antigen (Mac-1) receptor commonly used as a myeloid cell marker. CD11b is expressed on immune cells such as monocytes, macrophages, neutrophils, and NK cell subsets, and is known to play a role in regulating cell adhesion, migration, and phagocytosis ().
Figure 1. Typical EasySep? Human CD11b+ Positive Selection Profile
Starting with human PBMCs, the CD11b+ cell content of the isolated fraction is typically 98.6 ± 1.4% after positive selection and 1.7 ± 1.2% after depletion (mean ± SD using the EasySep? magnet). In the above example, the frequencies of CD11b+ cells in the start, final isolated, and final depleted fractions are 47.8%, 99.4%, and 1.6%, 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.
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 (M?¤s). Although M?¤s are a major niche, myeloid-derived suppressor cells (MDSCs) are an alternative site for pathogen persistence. Both M?¤s 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-M?¤s 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.
Mouse monoclonal IgG1 antibody against human, rhesus, cynomolgus CD11b
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EasySep? Human CD11b Positive Selection and Depletion Kit
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