Coen Maas

Antibody response to aggregated human interferon alpha2b in wild-type and transgenic immune tolerant mice depends on type and level of aggregation.

A role for protein misfolding in immunogenicity of biopharmaceuticals.

Misfolded proteins activate factor XII in humans, leading to kallikrein formation without initiating coagulation.

Identification of fibronectin type I domains as amyloid-binding modules on tissue-type plasminogen activator and three homologs.

Physiological responses to protein aggregates: fibrinolysis, coagulation and inflammation (new roles for old factors).

Activated factor V is a cofactor for the activation of factor XI by thrombin in plasma.

Mast cells increase vascular permeability by heparin-initiated bradykinin formation in vivo.

The plasma contact system 2.0.

Immune responses against domain I of β(2)-glycoprotein I are driven by conformational changes: domain I of β(2)-glycoprotein I harbors a cryptic immunogenic epitope.

Regulatory mechanisms of the plasma contact system.

In vivo roles of factor XII.

PDGFRB promotes liver metastasis formation of mesenchymal-like colorectal tumor cells.

Zinc-dependent contact system activation induces vascular leakage and hypotension in rodents.

New insights into the role of erythrocytes in thrombus formation.

FLow-induced PRotrusions (FLIPRs): a platelet-derived platform for the retrieval of microparticles by monocytes and neutrophils.

Plasmin Cleavage of von Willebrand Factor as an Emergency Bypass for ADAMTS13 Deficiency in Thrombotic Microangiopathy.

Plasma contact system activation drives anaphylaxis in severe mast cell-mediated allergic reactions.

A novel FcγRIIa Q27W gene variant is associated with common variable immune deficiency through defective FcγRIIa downstream signaling.

Endocannabinoids control platelet activation and limit aggregate formation under flow.

Contact system activation on endothelial cells.

Response to letter regarding article, "plasmin cleavage of von willebrand factor as an emergency bypass for ADAMTS13 deficiency in thrombotic microangiopathy".

In Vitro Hemocompatibility Testing of Dyneema Purity Fibers in Blood Contact.

Defective glycosylation of coagulation factor XII underlies hereditary angioedema type III.

Invasive surgery reduces infarct size and preserves cardiac function in a porcine model of myocardial infarction.

Keeping von Willebrand Factor under Control: Alternatives for ADAMTS13.

Coagulation Factor XI Promotes Distal Platelet Activation and Single Platelet Consumption in the Bloodstream Under Shear Flow.

Bradykinin: Inflammatory Product of the Coagulation System.

Plasmin is a natural trigger for bradykinin production in patients with hereditary angioedema with factor XII mutations.

Neutralizing blood-borne polyphosphate in vivo provides safe thromboprotection.

A flow cytometry-based assay for procoagulant platelet polyphosphate.

Processing of Factor XII during Inflammatory Reactions.

Polyphosphate strikes back.

Iron nanomedicines induce Toll-like receptor activation, cytokine production and complement activation.

Anti-histone Properties of C1 Esterase Inhibitor Protect Against Lung Injury.

Polyphosphate nanoparticles on the platelet surface trigger contact system activation.