Treatment of MCPT8DTR mice with high- or low-dose diphtheria toxin leads to differential depletion of basophils and granulocyte-macrophage progenitors.
Carole El HachemPierre HenerPeggy KirstetterJiagui LiSusan ChanMei LiPublished in: European journal of immunology (2018)
Basophils have been recently recognized to play important roles in type 2 immune responses during allergies and parasitic infection, largely due to the development of novel tools for the in vivo study of these cells. As such, the genetically-engineered MCPT8DTR mouse line has been used to specifically deplete basophils following treatment with diphtheria toxin (DT). In this study, we showed that DT-injected MCPT8DTR mice exhibited a striking decrease of eosinophils and neutrophils in skin when subjected to a hapten fluorescein isothiocyanate (FITC)-induced allergic contact dermatitis (ACD) experimental protocol. Unexpectedly, we found that loss of skin eosinophils and neutrophils was not due to a lack of basophil-mediated recruitment, as DT injection caused a systemic reduction of eosinophils and neutrophils in MCPT8DTR mice in a time-dependent manner. Furthermore, we found that hematopoietic stem-cell-derived granulocyte-macrophage progenitors (GMPs) expressed MCPT8 gene, and that these cells were depleted upon DT injection. Finally, we optimized a protocol in which a low-dose DT achieved a better specificity for depleting basophils, but not GMPs, in MCPT8DTR mice, and demonstrate that basophils do not play a major role in recruiting eosinophils and neutrophils to ACD skin. These data provide new and valuable information about functional studies of basophils.
Keyphrases
- low dose
- high fat diet induced
- induced apoptosis
- escherichia coli
- immune response
- soft tissue
- cell cycle arrest
- randomized controlled trial
- genome wide
- cell death
- machine learning
- healthcare
- insulin resistance
- wound healing
- copy number
- gene expression
- oxidative stress
- ultrasound guided
- big data
- skeletal muscle
- endothelial cells
- artificial intelligence
- dna methylation