Extended Data Fig. 6: Anti-MICL antibodies exacerbate autoinflammatory diseases.

a, ROS generation by MSU (left) or zymosan (right) of neutrophils derived from WT animals in the presence/absence of antibodies targeting MICL (αMICL) depicted as relative light units (RLU) over time. Data is a representative example of n = 2 independent experiments, mean ± SD performed in triplicate. b, Schematic and severity scoring of the GSK484 treatment regime during CAIA in the presence of anti-MICL or isotype control monoclonal antibodies. Severity scoring is shown as mean ± SD, n = 1 experiment with 3 mice/group. c, Schematic, severity scoring and cell recruitment in the inflamed joints at day 35 during CIA model. Severity scoring is shown as mean ± SD, n = 1 experiment with 6 mice/group, myeloid cell populations are represented as a percentage of total live cells. Statistical significance determined by two-way ANOVA with Tukey’s post hoc test. Schematics in panels b,c were created using BioRender (https://biorender.com). d, Level of anti-MICL autoantibodies in serum from healthy controls (HC) and RA patients used to stimulate human neutrophils in Fig. 3c. e, ROS generation by MSU of human neutrophils in the presence of serum from SLE patients and healthy controls (HC). Data is a representative example of n = 2 independent experiments, mean ± SD performed in triplicate. f, ROS generation by MSU of human neutrophils in the presence of pooled serum from sCOVID-19 patients and healthy controls (HC). Data is a representative example of n = 2 independent experiments, mean ± SD performed in triplicate. g, ROS generation and area under curve (AUC) of human neutrophils stimulated with MSU in the presence of pooled serum from sCOVID-19 patients pre-incubated with Fc-hMICL or Fc-control. Data is a representative example of n = 2 independent experiments, mean ± SD performed in triplicate. WT, wild-type mice; KO, MICL^−/− mice; ns, not significant; *, p < 0.05.

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