Fig. 4: NET–MICL interaction regulates inflammation.
From: Recognition and control of neutrophil extracellular trap formation by MICL
a, ROS generation by bone marrow neutrophils stimulated with preformed NETs, depicted as RLU over time. Data are a representative example of n = 4 independent experiments, depicted as mean ± s.d. performed in triplicate. mNET, preformed mouse NETs. b, Immunofluorescence staining for MPO (yellow), cit-H3 (magenta) and DNA (DAPI; grey) of neutrophils stimulated with preformed NETs. Scale bars, 200 µm. Quantification is in Extended Data Fig. 7b. c, ROS generation by human neutrophils stimulated with preformed NETs in the presence or absence of antibodies targeting MICL. Data are a representative example of n = 2 independent experiments, depicted as mean ± s.d. performed in duplicate. hPMNs versus anti-hMICL P = 0.0011 and anti-hMICL versus isotype P = 0.0016. d, Fc–MICL recognition of untreated NETs (NETs), proteinase K-treated (+prot K) or DNase-treated (+DNase I) NETs by ELISA. e, MICL-expressing BWZ reporter cell recognition of untreated NETs, proteinase K-treated or DNase-treated NETs. OD, optical density. Pooled data from two independent experiments, depicted as mean ± s.d. performed in triplicate (d,e). f, Neutrophil infiltration (CD45+CD11b+Ly6G+ cells) 4 h after preformed NETs or LPS injection in the peritoneum of WT and Micl−/− mice. Pooled data are from two independent experiments (n = 9 mice per group), depicted as mean ± s.d. NETs WT versus Micl−/− P = 0.0384. *P < 0.05, **P < 0.01 and ****P < 0.0001.
