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Organic compounds that exhibit highly efficient, stable blue emission are required to realize inexpensive organic light-emitting diodes for future displays and lighting applications. Here, we define the design rules for increasing the electroluminescence efficiency of blue-emitting organic molecules that exhibit thermally activated delayed fluorescence. We show that a large delocalization of the highest occupied molecular orbital and lowest unoccupied molecular orbital in these charge-transfer compounds enhances the rate of radiative decay considerably by inducing a large oscillator strength even when there is a small overlap between the two wavefunctions. A compound based on our design principles exhibited a high rate of fluorescence decay and efficient up-conversion of triplet excitons into singlet excited states, leading to both photoluminescence and internal electroluminescence quantum yields of nearly 100%.

Fluorescence-based organic light-emitting diodes have continued to attract interest because of their long operational lifetimes, high colour purity of electroluminescence and potential to be manufactured at low cost in next-generation full-colour display and lighting applications. In fluorescent molecules, however, the exciton production efficiency is limited to 25% due to the deactivation of triplet excitons. Here we report fluorescence-based organic light-emitting diodes that realize external quantum efficiencies as high as 13.4-18% for blue, green, yellow and red emission, indicating that the exciton production efficiency reached nearly 100%. The high performance is enabled by utilization of thermally activated delayed fluorescence molecules as assistant dopants that permit efficient transfer of all electrically generated singlet and triplet excitons from the assistant dopants to the fluorescent emitters. Organic light-emitting diodes employing this exciton harvesting process provide freedom for the selection of emitters from a wide variety of conventional fluorescent molecules.

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Allergic asthma is caused by the aberrant expansion in the lung of T helper cells that produce type 2 (TH2) cytokines and is characterized by infiltration of eosinophils and bronchial hyperreactivity. This disease is often triggered by mast cells activated by immunoglobulin E (IgE)-mediated allergic challenge. Activated mast cells release various chemical mediators, including prostaglandin D2 (PGD2), whose role in allergic asthma has now been investigated by the generation of mice deficient in the PGD receptor (DP). Sensitization and aerosol challenge of the homozygous mutant (DP-/-) mice with ovalbumin (OVA) induced increases in the serum concentration of IgE similar to those in wild-type mice subjected to this model of asthma. However, the concentrations of TH2 cytokines and the extent of lymphocyte accumulation in the lung of OVA-challenged DP-/- mice were greatly reduced compared with those in wild-type animals. Moreover, DP-/- mice showed only marginal infiltration of eosinophils and failed to develop airway hyperreactivity. Thus, PGD2 functions as a mast cell-derived mediator to trigger asthmatic responses.