Susanne Pfeiler

TL;DR: Deep vein thrombosis initiation is mediated by cross talk between monocytes, neutrophils, and platelets.

TL;DR: The ability of coagulation to suppress pathogen dissemination indicates that microvessel thrombosis represents a physiological tool of host defense, although the molecular determinants and in vivo significance of this association remain unclear.

TL;DR: Results support the hypothesis that vascular inflammation may be aggravated by oxLDL induced DC-activation and induces a proinflammatory cytokine profile in human DCs leading to DC-maturation and -differentiation which can be explained by an activation of the NF-kappaB-pathway.

TL;DR: During infections and in response to blood vessel damage, neutrophils and externalized nucleosomes are major promoters of intravascular blood coagulation and thrombosis.

TL;DR: GPVI activation results in differential changes in abundance of platelet proteins, including AR and ERp57, which support platelet aggregation and platelet-dependent coagulation, which provide further insight into the mechanisms that underlie platelet activation through the GPVI receptor.