Kristina Maaetoft-Udsen

TL;DR: Investigation of the aryl hydrocarbon receptor in model mast cells found that calcium influxes and mast cell secretory responses were enhanced or suppressed after chronic treatment with AHR agonists or antagonists, and that AHR ligands modified RBL2H3 cell degranulation.

TL;DR: Unbiased analysis of the impact of the presence of LB on the rate of trans-cytoplasmic calcium signals suggest that LB enrichment accelerates calcium propagation, which may reflect a Bernoulli effect.

TL;DR: The idea that the diagnosis of dioxin exposure, the subtleties of the cellular effects of the compounds and prognosis of the long‐term effects of exposure are problems requiring that researchers leverage the power of genomics and epigenetics is developed.

TL;DR: The hypothesis that insulin may regulate lipid body content in mast cells and hence, modify their proinflammatory potential is tested and data show that insulin causes lipid body accumulation in RBL2H3 and BMMCs.

TL;DR: It is demonstrated that in vivo hyperinsulinemia resulting from high fat diet is associated with LB accumulation in murine mast cells and basophils, and lipidomic analysis suggests a gain of function associated withLB accumulation, in terms of elevated levels of eicosanoid precursors that translate to enhanced antigen-induced LTC4 release.