Fig. 4: R69-4 reduces neutrophil FCGR3 (CD16) rapidly both in vivo and in vitro. | Nature Communications

Fig. 4: R69-4 reduces neutrophil FCGR3 (CD16) rapidly both in vivo and in vitro.

From: A subset of type-II collagen-binding antibodies prevents experimental arthritis by inhibiting FCGR3 signaling in neutrophils

Fig. 4

a R69-4 downregulated FCGR3 expression particularly on SF neutrophils 24 h after injection (Mann–Whitney U test, two-sided); Data shown as median ± IQR; b FCGR3 expression was downregulated in a spatial manner 8 h after R69-4 injection (pannus tissue (PT) <synovial fluid (SF) <peripheral blood (PB)); negative control (NC): PB lymphocytes; c Representative plots indicating that 8 h after R69-4 injection, majority of FCGR3 (CD16)low neutrophils were not apoptotic (Annexin-V+) in SF; d SF neutrophils from mice treated with R69-4 lost competence in phagocytosing IgG2b particles (Green); scale bar: 5 µm. e R69-4 reduced SF neutrophil FCGR3 expression efficiently after 1 h of incubation in vitro in a dose-dependent manner, and the lowest dose of R69-4 downregulated neutrophil FCGR3 expression significantly compared to the isotype control (M2139) (Two-way ANOVA); Data shown as mean + SD; f SF neutrophils from inflamed CAIA mice exhibited a rapid burst and exhaustion pattern of FCGR3 after incubation with R69-4 (100 µg/ml) but not with the isotype control (M2139) in vitro (Two-way ANOVA); Data shown as mean + SD. g SF neutrophils collected from CAIA + R69-4 mice displayed incompetence in responding to R69-4 (100 µg/ml) in vitro (Two-way ANOVA); Data shown as mean + SD. MFI median fluorescent intensity.

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