A Legacy of Lies: Examining Donald Trump’s Record-Breaking Dishonesty

Donald Trump told a record number of lies while in office, and ended his term with an unprecedent attack on democracy carried out by his supporters. Presidential lying has a long history in the United States, and significant research has been done on intention, lie typology, and outcomes. Trump’s lies go beyond the existing literature, threatening norms of democracy and bordering on authoritarian behavior. My research examines the power of presidential rhetoric by analyzing a dataset of fact-checked tweets, with the intention of better understanding if and how Trump’s dishonesty violates democratic norms and its potential implications for political violence. I find that this presidential lying falls outside of known typologies, with the unprecedented effect of undermining core democratic institutions and threatening the legitimacy of the American government. Trump uses anti-democratic call-to-action rhetoric that challenges the widely accepted norms of democracy, widening the scope of acceptable presidential behavior and eroding public trust in government

Podoplanin-rich stromal networks induce dendritic cell motility via activation of the C-type lectin receptor CLEC-2

To initiate adaptive immunity, dendritic cells (DCs) move from parenchymal tissues to lymphoid organs by migrating along stromal scaffolds that display the glycoprotein podoplanin (PDPN). PDPN is expressed by lymphatic endothelial and fibroblastic reticular cells and promotes blood-lymph separation during development by activating the C-type lectin receptor, CLEC-2, on platelets. Here, we describe a role for CLEC-2 in the morphodynamic behavior and motility of DCs. CLEC-2 deficiency in DCs impaired their entry into lymphatics and trafficking to and within lymph nodes, thereby reducing T cell priming. CLEC-2 engagement of PDPN was necessary for DCs to spread and migrate along stromal surfaces and sufficient to induce membrane protrusions. CLEC-2 activation triggered cell spreading via downregulation of RhoA activity and myosin light-chain phosphorylation and triggered F-actin-rich protrusions via Vav signaling and Rac1 activation. Thus, activation of CLEC-2 by PDPN rearranges the actin cytoskeleton in DCs to promote efficient motility along stromal surfaces