Programmed death ligand 1 (PD-L1), a type I transmembrane protein, binds to its receptor PD-1 to suppress the activation of T cells, thereby maintaining immunological homeostasis. In contrast, tumor cells highly express PD-L1, which binds to receptor PD-1 expressed on activated T cells, leading to immune escape. Anti-PD-1/PD-L1 immune checkpoint therapy blocks the binding of PD-1/PD-L1 to reinvigorate the exhausted T cells, thereby inhibiting tumor growth. Exosomes are biologically active lipid-bilayer nanovesicles secreted by various cell types that mediate intercellular signal communication. Numerous studies have shown that tumor cells are able to promote tumor epithelial-mesenchymal transition, angiogenesis, and immune escape by releasing exosomes. Recent studies imply that tumor-derived exosomes could carry PD-L1 in the same membrane topology as the cell surface, thereby resisting immune checkpoint therapy. In this review, we mainly discuss the role of exosomes in the regulation of tumor progression and the potential resistance mechanism to immunotherapy via exosomal PD-L1. In addition, we propose that exosomal PD-L1 may have the potential to be a target to overcome resistance to anti-PD-1/PD-L1 antibody therapy.

The research of carbon-based antivirals is still in its infancy, and their development into safe and effective carbon dots (CDs) with antiviral activity at multiple points in the life cycle of the virus remains to be explored. Here, we report a one-step method to apply curcumin in order to prepare of uniform and stable cationic carbon dots (CCM-CDs) with antiviral properties. The inhibitory effect of CCM-CDs on viral replication was studied by using porcine epidemic diarrhea virus (PEDV) as a coronavirus model. PEDV is applied as a coronavirus model to study the antiviral effect of as-prepared CCM-CDs on its replication. The cationic CCM-CDs treatment is found obviously to inhibit the proliferation of PEDV compared with the common CDs (EDA-CDs). The CCM-CDs treatment can change the structure of surface protein in viruses, thereby inhibiting viral entry. It can also suppresses the synthesis of negative-strand RNA of the virus, the budding of the virus, and the accumulation of reactive oxygen species by PEDV. Furthermore, CCM-CDs treatment is also found to suppress viral replication by stimulating the production of interferon-stimulating genes (ISGs) and proinflammatory cytokines. These results offer theoretical support for the development of CCM-CDs as a hopeful antiviral drug for the treatment of coronavirus infections, including PEDV.

Development of novel antiviral reagents is of great importance for the control of virus spread. Here, AgS nanoclusters (NCs) were proved for the first time to possess highly efficient antiviral activity by using porcine epidemic diarrhea virus (PEDV) as a model of coronavirus. Analyses of virus titers showed that AgS NCs significantly suppressed the infection of PEDV by about 3 orders of magnitude at the noncytotoxic concentration at 12 h postinfection, which was further confirmed by the expression of viral proteins. Mechanism investigations indicated that AgS NCs treatment inhibits the synthesis of viral negative-strand RNA and viral budding. AgS NCs treatment was also found to positively regulate the generation of IFN-stimulating genes (ISGs) and the expression of proinflammation cytokines, which might prevent PEDV infection. This study suggest the novel underlying of AgS NCs as a promising therapeutic drug for coronavirus.

Developing nanomaterials-based antimicrobial agents has shown a widespread promise. In this study, silver nanoparticle-modified graphene oxide (GO-AgNPs) nanocomposites were self-assembled via interfacial electrostatic force. By using the porcine reproductive and respiratory syndrome virus (PRRSV) as a pattern, the antiviral effect of the as-prepared GO-AgNPs nanocomposites on the replication of virus was investigated. The results indicated that exposure with GO-AgNPs nanocomposites could obviously suppress PRRSV infection. It was found that GO-AgNPs nanocomposites exhibited a better inhibitory effect compared with AgNPs and GO. By selecting the porcine epidemic diarrhea virus (PEDV) as a contrast virus, GO-AgNPs nanocomposites were proven to have a broad antiviral activity. Mechanism studies showed that GO-AgNPs nanocomposites might prevent PRRSV from entering the host cells, with 59.2% inhibition efficiency. Meanwhile, GO-AgNPs nanocomposite treatment enhances the production of interferon-α (IFN-α) and IFN-stimulating genes (ISGs), which can directly inhibit the proliferation of virus. Taken together, this study reports a new type of antiviral agent and provides a promising pharmaceutical agent for treating infection by the highly pathogenic PRRSV. Moreover, it may provide novel ideas for the research and development of antiviral formulations based on nanocomposites and extend their applications in biological systems.

Exposure of the skin to ultraviolet B (UVB) radiation causes oxidative damage to skin, resulting in sunburn, photoaging, and skin cancer. It is generally believed that the skin damage induced by UV irradiation is a consequence of generation of reactive oxygen species (ROS). Recently, there is an increased interest in the use of natural products as chemopreventive agents for non-melanoma skin cancer (NMSC) due to their antioxidants and anti-inflammatory properties. Quercitrin, glycosylated form of quercetin, is the most common flavonoid in nature with antioxidant properties. The present study investigated the possible beneficial effects of quercitrin to inhibit UVB irradiation-induced oxidative damage in vitro and in vivo. Our results showed that quercitrin decreased ROS generation induced by UVB irradiation in JB6 cells. Quercitrin restored catalase expression and GSH/GSSG ratio reduced by UVB exposure, two major antioxidant enzymes, leading to reductions of oxidative DNA damage and apoptosis and protection of the skin from inflammation caused by UVB exposure. The present study demonstrated that quercitrin functions as an antioxidant against UVB irradiation-induced oxidative damage to skin.