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• W2783190828 endingPage "873" @default.
• W2783190828 startingPage "861" @default.
• W2783190828 abstract "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." @default.
• W2783190828 created "2018-01-26" @default.
• W2783190828 creator A5002125195 @default.
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• W2783190828 date "2018-01-29" @default.
• W2783190828 modified "2023-10-18" @default.
• W2783190828 title "Treatment of MCPT8^DTR mice with high- or low-dose diphtheria toxin leads to differential depletion of basophils and granulocyte-macrophage progenitors" @default.
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• W2783190828 doi "https://doi.org/10.1002/eji.201747351" @default.
• W2783190828 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/29315532" @default.
• W2783190828 hasPublicationYear "2018" @default.
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