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. 2017 Apr 20;189(2):250–258. doi: 10.1111/cei.12970

Figure 1.

Figure 1

Effect of Janus kinase (JAK) inhibition on neutrophil apoptosis. Neutrophils from healthy controls (a,b) and (c) rheumatoid arthritis (RA) patients were incubated with baricitinib or tofacitinib over a range of concentrations (50–200 ng/ml) for 30 min prior to addition of granulocyte–macrophage‐colony stimulating factor (GM‐CSF) (5 ng/ml) or interferon (IFN)‐γ, 10 ng/ml) for 20 h. Dimethylsulphoxide (DMSO) was used as a vehicle control. (a) GM‐CSF‐ and IFN‐γ‐delayed apoptosis (§P < 0·01) was abrogated by baricitinib and tofacitinib in a dose‐dependent manner (*P < 0·05, **P < 0·01). (b) Phosphorylation of signal transducer and activator of transcription (STAT)‐3 by GM‐CSF and STAT‐1 by IFN‐γ occurred after 15 min incubation, and was inhibited by high concentrations of baricitinib and tofacitinib (n = 3, *P < 0·05). (c) GM‐CSF‐delayed apoptosis was abrogated by baricitinib and tofacitinib (200 ng/ml) in RA neutrophils (*P < 0·05; **P < 0·01).