Desai J, Kumar SV, Mulay SR, Konrad L, Romoli S, Schauer C, Herrmann M, Bilyy R, Mueller S, Popper B, Nakazawa D, Weidenbusch M, Thomasova D, Krautwald S, Linkermann A, Anders HJ (2016)
Publication Type: Journal article
Publication year: 2016
Book Volume: 46
Pages Range: 223-9
Journal Issue: 1
Neutrophil extracellular trap (NET) formation contributes to gout, autoimmune vasculitis, thrombosis, and atherosclerosis. The outside-in signaling pathway triggering NET formation is unknown. Here, we show that the receptor-interacting protein kinase (RIPK)-1-stabilizers necrostatin-1 or necrostatin-1s and the mixed lineage kinase domain-like (MLKL)-inhibitor necrosulfonamide prevent monosodium urate (MSU) crystal- or PMA-induced NET formation in human and mouse neutrophils. These compounds do not affect PMA- or urate crystal-induced production of ROS. Moreover, neutrophils of chronic granulomatous disease patients are shown to lack PMA-induced MLKL phosphorylation. Genetic deficiency of RIPK3 in mice prevents MSU crystal-induced NET formation in vitro and in vivo. Thus, neutrophil death and NET formation may involve the signaling pathway defining necroptosis downstream of ROS production. These data imply that RIPK1, RIPK3, and MLKL could represent molecular targets in gout or other crystallopathies.
APA:
Desai, J., Kumar, S.V., Mulay, S.R., Konrad, L., Romoli, S., Schauer, C.,... Anders, H.-J. (2016). PMA and crystal-induced neutrophil extracellular trap formation involves RIPK1-RIPK3-MLKL signaling. European Journal of Immunology, 46(1), 223-9. https://doi.org/10.1002/eji.201545605
MLA:
Desai, Jyaysi, et al. "PMA and crystal-induced neutrophil extracellular trap formation involves RIPK1-RIPK3-MLKL signaling." European Journal of Immunology 46.1 (2016): 223-9.
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