Interactions between pathogens, the immune system, and coagulation are multifaceted and overlapping. Ideally, pathogens and pathogen-derived molecules activate coagulation factors and platelets resulting in the enhancement of the host immune response and the generation of localized thrombi that limit pathogen dissemination. These responses, however, also have the capacity to trigger disseminated coagulopathies and the generation of biofilms, complex structures that shield the pathogen from the immune system, promote bacterial adhesion, and support the persistence of infection. Importantly, these pathways do not exist in isolation, activation of the immune response can further drive coagulation, and events such as thrombin generation can further potentiate the inflammatory response. CR, complement receptor; FCR, Fc receptor; NET, neutrophil extracellular trap.

Interactions between pathogens, the immune system, and coagulation are multifaceted and overlapping. Ideally, pathogens and pathogen-derived molecules activate coagulation factors and platelets resulting in the enhancement of the host immune response and the generation of localized thrombi that limit pathogen dissemination. These responses, however, also have the capacity to trigger disseminated coagulopathies and the generation of biofilms, complex structures that shield the pathogen from the immune system, promote bacterial adhesion, and support the persistence of infection. Importantly, these pathways do not exist in isolation, activation of the immune response can further drive coagulation, and events such as thrombin generation can further potentiate the inflammatory response. CR, complement receptor; FCR, Fc receptor; NET, neutrophil extracellular trap.

Close Modal

or Create an Account

Close Modal
Close Modal