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Background Immune complex (IC)-mediated formation of neutrophil extracellular traps (NETs) has emerged as a mechanism to increase the autoantigenic burden as well as promote the prominent type I interferon (IFN) signature seen in patients with the autoimmune disease systemic lupus erythematosus (SLE). The aim of the current study was to explore properties of ICs regulating their ability to induce phagocytosis and NETosis.
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