Interleukin-18 diagnostically distinguishes and pathogenically promotes human and murine macrophage activation syndrome
Eric S. Weiss(University of Pittsburgh), Charlotte Girard(University Hospital of Geneva), Dirk Holzinger(University Hospital Münster), Adriana A. de Jesus(National Institute of Allergy and Infectious Diseases), Zeshan Tariq(National Institutes of Health), Jennifer Picarsic(Children's Hospital of Pittsburgh), Eduardo J. Schiffrin(AB2 Bio (Switzerland)), Dirk Foell(University Hospital Münster), Alexei A. Grom(Cincinnati Children's Hospital Medical Center), Sandra Ammann(University of Freiburg), Stephan Ehl(University of Freiburg), Tomoaki Hoshino(Kurume University), Raphaela Goldbach‐Mansky(National Institute of Allergy and Infectious Diseases), Cem Gabay(University Hospital of Geneva), Scott Canna(University of Pittsburgh)
Cited by 392Open Access
Abstract
mice, whose free IL-18 levels were normal, did not. Thus, we describe a unique connection between MAS risk and chronic IL-18, identify epithelial inflammasome hyperactivity as a potential source, and demonstrate the pathogenicity of free IL-18. These data suggest an IL-18-driven pathway, complementary to the cytotoxic impairment of fHLH, with potential as a distinguishing biomarker and therapeutic target in MAS.
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