Fig. 3: R69-4 abrogates acute granulopoiesis and quenches IL-1β secretion.

a Representative plots showing rapid and potent suppression on neutrophil expansion 24 h after R69-4 injection in CAIA; Events gated from live single CD11b⁺ peripheral blood mononuclear cells (PBMCs); proportions indicate the percentage of neutrophils in CD11b⁺ cells. b R69-4 lowered mouse neutrophil proportion of white blood cells (WBCs) in CAIA from d2 to d4 (Two-way ANOVA); Data shown as mean + SD; c Mice injected with R69-4 had lower neutrophil absolute counts in PBMCs than that of the untreated CAIA controls (Mann–Whitney U test, two-sided); Data shown as median ± inter-quartile range (IQR). d Mice injected with R69-4 had lower neutrophil absolute counts in synovial fluid (SF) than that of the untreated CAIA controls (Mann–Whitney U test, two-sided); Data shown as median ± IQR. e Mice treated with R69-4 demonstrated lower level of IL-1β in SF than that of the untreated CAIA counterparts (Mann–Whitney U test, two-sided); Data shown as median ± IQR. f Recombinant IL-1β injection failed to reconstitute disease completely prevented by R69-4; R69-4: 1 mg, d-1, i.v.; Cab4: 2 mg, d0, i.v.; IL-1β: 2.5 µg in PBS containing 0.2% bovine serum albumin (BSA, carrier protein), d1, i.p., same volume of carrier protein was injected to the other two groups; No difference was recorded regarding arthritis severity between the two groups receiving R69-4 (Two-way ANOVA); Data shown as mean + SD. g Representative plots showing that the injected recombinant IL-1β was biologically active, which stimulated the release of immature neutrophils into periphery; Events gated from live single CD11b⁺ PBMCs; proportions indicate the percentage of neutrophils in CD11b⁺ population.