HITing back against NETs

In this issue of Blood, Gollomp et al demonstrate that a monoclonal antibody (KKO) with properties resembling those of antibodies from patients with heparin-induced thrombocytopenia (HIT) can be deglycosylated and used therapeutically to improve outcomes in a murine model of sepsis.(1) The mechanism underlying this activity appears to involve contraction and stabilization of neutrophil extracellular traps (NETs) and suggests a novel approach to the management of sepsis, which is associated with a mortality of 30% and an annual cost exceeding 20 billion dollars in the United States.(2)