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A History of Flow Cytometry and Sorting
Published in Frances S. Ligler, Jason S. Kim, The Microflow Cytometer, 2019
Since the 1980s, an increasingly wide range of fluorescent labels of different types have become available, including low molecular weight dyes, phycobilipro- teins, phycobiliprotein-dye tandem conjugates, and, most recently, semiconductor nanocrystals, more popularly known as quantum dots; many of these labels can be used with ligands other than antibodies, e.g., nucleic acid sequence probes. A series of international workshops has defined several hundred "CD" (Cluster of Differentiation) antigens that are expressed on various cell types, and directly conjugated fluorescent antibodies to many of these are widely available. Perhaps the best known example of a CD antigen is CD4, expressed (with CD3) on the helper subset of T lymphocytes, which are the target cells for HIV, the human immunodeficiency virus; counts of patients' CD4-positive T cells are routine done to monitor therapy of HIV/AIDS wherever the technology (most commonly fluorescence flow cytometry) is supportable and affordable, and much current work on miniaturized flow cytometers has been motivated by the goal of producing CD4 counters suitable for use in resource-poor countries.50
Visualizing Hepatic Immunity through the Eyes of Intravital Microscopy
Published in Margarida M. Barroso, Xavier Intes, In Vivo, 2020
Maria Alice Freitas-Lopes, Maísa Mota Antunes, Raquel Carvalho-Gontijo, Érika de Carvalho, Gustavo Batista Menezes
Many immune cell markers are named following the clusters of differentiation (CD) nomenclature, which aims to provide targets for cell immunophenotyping. The majority of these surface antigens is not only specific to a unique cell type. A classic example is the CD11b, an integrin family member, expressed on the surface of many leukocytes including monocytes, neutrophils, NK cells, granulocytes, and macrophages. To better identify a specific cell type, it is important to search for a marker expressed exclusively for this lineage or cell. Additionally, imaging experiments allow the evaluation of morphological aspects of the cells, as well as the size and presence of dendrites, for example, which facilitates their identification jointly to the marking.
Glossary of scientific and technical terms in bioengineering and biological engineering
Published in Megh R. Goyal, Scientific and Technical Terms in Bioengineering and Biological Engineering, 2018
Cluster of differentiation (cluster of designation or Classification Determinant, CD) is a protocol used for the identification and investigation of cell surface molecules providing targets for immunophenotyping of cells.
Benzo[a]pyrene osteotoxicity and the regulatory roles of genetic and epigenetic factors: A review
Published in Critical Reviews in Environmental Science and Technology, 2022
Jiezhang Mo, Doris Wai-Ting Au, Jiahua Guo, Christoph Winkler, Richard Yuen-Chong Kong, Frauke Seemann
MiR-29 promotes OC commitment by targeting nuclear factor I/A (NFIA), G protein–coupled receptor 85 (GPR85), and the cluster of differentiation 93 (CD93) (Franceschetti et al., 2013). MiR-106b and miR-338 inhibit OC differentiation by targeting RANKL (Wang et al., 2015; Zhang, Geng et al., 2016), while miR-34c promotes OC differentiation by targeting leucine-rich repeat-containing G protein-coupled receptor 4 (LGR4), which can compete for RANKL (Cong et al., 2017). MiR-144 and miR-503 inhibit OC differentiation by targeting RANK (Chen et al., 2014; Wang, He, et al., 2018), whereas miR-145 promotes OC differentiation by targeting OPG (Chen et al., 2018). The upregulation of miR-148a supports OC differentiation by targeting V-maf musculoaponeurotic fibrosarcoma oncogene homolog B (MAFB) to activate NFATc1 expression (Cheng et al., 2013). OC differentiation is promoted by NF-κB activation via the downregulation of miR-145 and miR-99b, which stimulates the upregulation of their targets, SMAD3 and insulin-like growth factor 1 receptor (IGFLR) (de la Rica et al., 2015; Yu et al., 2018).
The expression of microRNAs and exposure to environmental contaminants related to human health: a review
Published in International Journal of Environmental Health Research, 2022
Maria Rosaria Tumolo, Alessandra Panico, Antonella De Donno, Pierpaolo Mincarone, Carlo Giacomo Leo, Roberto Guarino, Francesco Bagordo, Francesca Serio, Adele Idolo, Tiziana Grassi, Saverio Sabina
Air pollution could alter intercellular communication by extracellular vesicles (EVs), such as MVs, that can transfer miRNAs between tissues (Pavanello et al. 2016). Rodosthenous et al. investigated relationship between short-, intermediate-, and long-term exposures to PM and levels of EV-miRNAs in a cohort of healthy adults. The profile of 800 miRNAs was screened using Nanostring Technologies’ nCounter® assay that revealed an association between long-term ambient PM exposure with increased levels of some EV – miRNAs circulating in serum; in silico analysis showed that their target genes (for example interleukin 6 – IL-6, C-X-C motif chemokine ligand 12 – CXCL12, vascular cell adhesion molecule 1 – VCAM-1, cluster of differentiation 40 – CD40, platelet-derived growth factor subunit beta – PDGFB, etc.) are linked to CVD-related pathways, such as inflammatory response, atherosclerosis, toll-like receptor (TLR) etc. (Rodosthenous et al. 2016).
Ozone exposure and pulmonary effects in panel and human clinical studies: Considerations for design and interpretation
Published in Journal of the Air & Waste Management Association, 2018
Frampton et al. (2017) exposed 87 older adults (ages 55–70 years) to either 0, 70, or 120 ppb ozone (randomized) for 3 hr in the MOSES (Multicenter Ozone Study in Older Subjects) study. During the exposures, participants exercised on a stationary bicycle, alternating 15 minutes of exercise with 15 minutes of rest. While the primary health outcomes were related to cardiovascular impacts, secondary outcomes included lung function decrements, airway inflammation as represented by sputum PMNs and soluble markers, and respiratory symptoms. Spirometry was conducted 30 min prior to exposure, immediately postexposure, and 1 day after exposure. Sputum was induced 1 day after exposure. Symptoms were evaluated 30 min prior to exposure, immediately postexposure, 3–4 hr postexposure, and 1 day after exposure. During clean air exposure, FEV1 and FVC increased compared with preexposure values, and this effect persisted the following day. These improvements in lung function were shown to be attenuated in a dose-dependent manner with ozone exposure. There were no changes in FEV1/FVC or FEF25-75, suggesting that bronchoconstriction was not occurring. A significant increase in the percent PMNs in sputum was noted 22 hr after exposure to 120 ppb ozone; no significant increase was observed after 70 ppb exposure. No significant changes in sputum cluster of differentiation 40 (CD40) ligand, interleukin-6 (IL-6), interleukin-8 (IL-8), tumor necrosis factor-α (TNF-α), or total protein were observed. Ozone exposures did not significantly affect respiratory symptoms.