Analyses of genome wide association data, cytokines, and gene expression in African-Americans with benign ethnic neutropenia.
Bashira A CharlesMatthew M HsiehAdebowale A AdeyemoDaniel ShrinerEdward RamosKyung ChinKshitij SrivastavaNeil A ZakaiMary CushmanLeslie A McClureVirginia HowardWilly A FlegelCharles N RotimiGriffin P RodgersPublished in: PloS one (2018)
These results in humans support the notion of DARC null erythroid progenitors preferentially differentiating to myeloid cells, leading to activated DARC null neutrophils egressing from circulation to the spleen, and causing relative neutropenia. Collectively, these human data sufficiently explained the mechanism DARC null red cell phenotype causing BEN and further provided a biologic basis that BEN is clinically benign.
Keyphrases
- gene expression
- genome wide association
- electronic health record
- induced apoptosis
- endothelial cells
- big data
- rheumatoid arthritis
- dna methylation
- single cell
- cell cycle arrest
- acute myeloid leukemia
- bone marrow
- cell therapy
- chemotherapy induced
- induced pluripotent stem cells
- stem cells
- machine learning
- mesenchymal stem cells
- magnetic resonance
- signaling pathway
- endoplasmic reticulum stress
- deep learning
- cell death
- artificial intelligence
- cell proliferation