Two novel evaporation- and solution-process-feasible thermally activated delayed fluorescence emitters, green-light-emission ACRDSO2 and yellow-light-emission PXZDSO2, based on a brand-new electron-acceptor moiety thianthrene-9,9',10,10'-tetraoxide, are developed for organic light-emitting diodes. The solution-processed devices, without any hole-transport layer, exhibit competitive performance and reduced efficiency roll-off compared with corresponding vacuum-deposited devices.

The type I interferon (IFN) response is part of the first-line defense against viral infection. To initiate replication, viruses have developed powerful evasion strategies to counteract host IFN responses. In the present study, we found that the Japanese encephalitis virus (JEV) NS5 protein could inhibit double-stranded RNA (dsRNA)-induced IFN-␤ expression in a dose-dependent manner. Our data further demonstrated that JEV NS5 suppressed the activation of the IFN transcriptional factors IFN regulatory factor 3 (IRF3) and NF-B. However, there was no defect in the phosphorylation of IRF3 and degradation of IB, an upstream inhibitor of NF-B, upon NS5 expression, indicating a direct inhibition of the nuclear localization of IRF3 and NF-B by NS5. Mechanistically, NS5 was shown to interact with the nuclear transport proteins KPNA2, KPNA3, and KPNA4, which competitively blocked the interaction of KPNA3 and KPNA4 with their cargo molecules, IRF3 and p65, a subunit of NF-B, and thus inhibited the nuclear translocation of IRF3 and NF-B. Furthermore, overexpression of KPNA3 and KPNA4 restored the activity of IRF3 and NF-B and increased the production of IFN-␤ in NS5-expressing or JEV-infected cells. Additionally, an upregulated replication level of JEV was shown upon KPNA3 or KPNA4 overexpression. These results suggest that JEV NS5 inhibits the induction of type I IFN by targeting KPNA3 and KPNA4.IMPORTANCE JEV is the major cause of viral encephalitis in South and Southeast Asia, with high mortality. However, the molecular mechanisms contributing to the severe pathogenesis are poorly understood. The ability of JEV to counteract the host innate immune response is potentially one of the mechanisms responsible for JEV virulence. Here we demonstrate the ability of JEV NS5 to interfere with the dsRNAinduced nuclear translocation of IRF3 and NF-B by competitively inhibiting the interaction of IRF3 and NF-B with nuclear transport proteins. Via this mechanism, JEV NS5 suppresses the induction of type I IFN and the antiviral response in host cells. These findings reveal a novel strategy for JEV to escape the host innate immune response and provide new insights into the pathogenesis of JEV.

Two thioxanthone‐derived isomeric series of thermally activated delayed fluorescence (TADF) emitters 1,6‐2TPA‐TX/3,6‐2TPA‐TX and 1,6‐2TPA‐TXO/3,6‐2TPA‐TXO are developed for organic light‐emitting diodes (OLEDs). Blue emission devices based on symmetrical 3,6‐2TPA‐TX with common vertical transition route realize an extremely high external quantum efficiency (EQE) of 23.7%, and an ever highest EQE of 24.3% is achieved for yellow emission devices based on 3,6‐2TPA‐TXO by solely changing the sulfur atom valence state of the thioxanthone core. In contrast, their corresponding asymmetric isomers are affected by intramolecular energy transfer and more severely by a nonradiative deactivation pathway, to give much low EQE values (<5%). By utilizing 3,6‐2TPA‐TX as a blue emitter and 3,6‐2TPA‐TXO as a yellow emitter, an ever highest EQE of 20.4% is achieved for all‐fluorescence white OLEDs.

Japanese encephalitis is a neuropathological disorder caused by Japanese encephalitis virus (JEV), which is characterized by severe pathological neuroinflammation and damage to the blood–brain barrier (BBB). Inflammatory cytokines/chemokines can regulate the expression of tight junction (TJ) proteins and are believed to be a leading cause of BBB disruption, but the specific mechanisms remain unclear. IP-10 is the most abundant chemokine produced in the early stage of JEV infection, but its role in BBB disruption is unknown. The administration of IP-10-neutralizing antibody ameliorated the decrease in TJ proteins and restored BBB integrity in JEV-infected mice. In vitro study showed IP-10 and JEV treatment did not directly alter the permeability of the monolayers of endothelial cells. However, IP-10 treatment promoted tumor necrosis factor alpha (TNF-α) production and IP-10-neutralizing antibody significantly reduced the production of TNF-α. Thus, TNF-α could be a downstream cytokine of IP-10, which decreased TJ proteins and damaged BBB integrity. Further study indicated that JEV infection can stimulate upregulation of the IP-10 receptor CXCR3 on astrocytes, resulting in TNF-α production through the JNK-c-Jun signaling pathway. Consequently, TNF-α affected the expression and cellular distribution of TJs in brain microvascular endothelial cells and led to BBB damage during JEV infection. Regarding regulation of the BBB, the IP-10/TNF-α cytokine axis could be considered a potential target for the development of novel therapeutics in BBB-related neurological diseases.

Thioxanthone derivatives consisting of undecorated carbazole as an electron donor and thioxanthone (TXO) or 9H-thioxanthen-9-one-S,S-dioxide (SOXO) as an electron acceptor in a donor-acceptor (D-A) or donor-acceptor-donor (D-A-D) structure were developed as thermally activated delayed fluorescence emitters to fabricate highly efficient fluorescent organic light emitting diodes. Their emission color was successfully tuned from blue to yellow by changing the sulfur atom valence state of the thioxanthone unit to tune intramolecular charge transfer effect. Their thermal, electrochemical, photophysical, and electroluminescent properties, and theoretical calculations were systematically investigated to illustrate the molecular structure and property relationships. Maximum external quantum efficiency (EQE) of 13.6% with Commission Internationale de L'Eclairage coordinates of (0.37, 0.57) was achieved for green light emission CzSOXO consisting of SOXO and carbazole in a D-A structure. Blue light emission CzTXO and DCzTXO consisting of TXO and carbazole in a D-A and D-A-D structure could also give EQE values exceeding 11%. Their efficiency roll-off with increasing current density was simulated by adopting triplet-triplet annihilation model, indicating that the TXO derivatives suffer more severe efficiency roll-off because of their relatively long delayed fluorescence lifetime (τ(D)).