NOX2 mediates quiescent handling of dead cell remnants in phagocytes.

A strong trend to increased intracellular accumulation of SNECs was also seen in Ncf1** neutrophils.

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Furthermore, plasma levels of SNEC-binding (anti-dsDNA) antibodies correlated with uptake of SNECs in neutrophils and showed a trend of a correlation in monocytes ( Fig. 1 E and F). 3.2 Dysfunction of the NOX2 complex causes accumulation of SNECS in murine phagocytes accompanied by increased production of inflammatory mediators To perform functional studies, we used the Ncf1** mouse strain which does not produce ROS via the NOX2 complex due to a mutation in the Ncf1 gene, one of the activating subunits of the NOX2 complex [ 27 , 28 ].

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However, spontaneous intracellular production of ROS in monocytes from patients with SLE appeared to show a weak trend to be negatively correlated with phagocytosis of SNECs ( Fig. 1 C and D).

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