Integrins are transmembrane receptors composed of alpha and beta chains, where beta-integrins are mainly expressed in leukocytes. Leukocytes are white blood cells that act in the immune system to defend our body against foreign pathogens. Integrins are known to interact with extracellular matrix molecules to initiate our inflammatory immune response, in addition to regulating cell adhesion, migration and proliferation. Our innate immune response is composed of a number of cell types that work in a coordinated effort to identify and attack foreign particles through antigen production. CD11b is expressed in macrophages, monocytes, dendritic cells and granulocytes – the main players of our immune response cell network. While CD11b’s exact role in immunity is still debated, it has been established that CD11b both negative and positively regulates our immune response, often times via a TLR ligand. The following research articles use a CD11b antibody in their immune based research.
CD11b Antibody [NB110-89474] - CD11b antibody was tested in Raw264.7 cells with Dylight 488 (green). Nuclei and alpha-tubulin were counterstained with DAPI (blue) and Dylight 550 (red).
First, Makar et al used a CD11b antibody to study the role of Abcc8 and reduced inflammation and disease progression in the autoimmune disorder encephalomyelitis (EAE). This group introduced EAE to wild-type and Abcc8 null mice and performed immunohistochemistry and immunoprecipitation on the tissue samples to collect analysis using primary antibodies. The CD11b antibody was used on the lumbar spinal cord tissue and showed that after 30 days, these tissues expressed smaller amounts of immune cells – including macrophages (indicated by the CD11b antibody). They also found that the Sur1-Trmp4 channels were upregulated, suggesting a novel therapeutic target for the treatment of EAE.
Next, Kim et al used a CD11b antibody to show that TLR9 stimulation in macrophages causes the release of extracellular CD11b. Prior research had established that CD11b facilitated TLR-initiated inflammatory responses in macrophages and dendritic cells, however the exact mechanism is unknown. The CD11b antibody was used in control Raw 264.7 macrophages or Raw 264.7 macrophages treated with CpG-DNA in western blot. The results showed that CpG-DNA, which stimulates TLR9, did cause release of CD11b. In addition, they found that this release was associated with exosomes.
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