New research suggests that extracorporeal photopheresis, a second-line treatment for graft-versus-host disease (GVHD), may function by inducing formation of neutrophil extracellular traps in patients with GVHD.
Idan Goldberg, MD, of the Institute of Hematology at the Davidoff Center for the Treatment and Research of Cancer, Beilinson Hospital, Rabin Medical Center in Petah Tikva, Israel, and colleagues conducted the study and presented its findings at the Tenth Annual Meeting of the Society of Hematologic Oncology.
Researchers conducted the study because the “mechanism by which [extracorporeal photopheresis] acts against GVHD is not fully understood,” Dr. Goldberg and colleagues wrote.
Researchers collected blood samples from 6 patients with chronic GVHD before extracorporeal photopheresis, at the end of the first day of extracorporeal photopheresis and 24 hours after the initiation of the extracorporeal photopheresis cycle. Most patients had acute myeloid leukemia (66%), while 1 had B-cell acute lymphocytic leukemia and 1 had myelodysplastic syndrome. Dr. Goldberg and colleagues assessed neutrophil extracellular trap formation by measuring neutrophil elastase activity and immunofluorescence.
There was a “sharp increase” in neutrophil extracellular trap formation in all patients after extracorporeal photopheresis, according to the researchers. The neutrophil elastase activity level increased from a mean baseline value of 2.21 mU/mL to a mean value of 13.82 mU/mL at the end of the first day of treatment, peaking at 17.35 mU/mL at 24 hours posttreatment.
“Our preliminary data indicate that [extracorporeal photopheresis] induces [neutrophil extracellular trap] formation among patients with GVHD,” Dr. Goldberg and colleagues concluded. “Given the central role of neutrophils in the pathogenesis of GVHD, the contribution of [neutrophil extracellular traps] to GVHD, and to [extracorporeal photopheresis’] mode of action, should be further investigated.”
Goldberg I, Granot G, Telerman A, et al. Extracorporeal photopheresis induces NETosis in neutrophils derived from patients with graft-versus-host disease. Poster CT-223. Presented at the Tenth Annual Meeting of the Society of Hematologic Oncology; September 28-October 1, 2022; Houston, TX.
