STAT3 Genotypic Variant rs744166 and Increased Tyrosine Phosphorylation of STAT3 in IL-23 Responsive Innate Lymphoid Cells during Pathogenesis of Crohn’s Disease

Figure 4

Activation of STAT3 signaling in innate lymphoid cells in response to IL-23 stimulation. (a) PBMCs from healthy donor were stimulated by 20 ng/ml of IL-23 for 15 minutes. After gating Lin^-CD45⁺CD127⁺CRTH2^- cells, the ILC population was further gated based on CD117 and NKp44 expression. The CD117⁺NKp44^- ILC3 population (NCR^-ILC3 phenotype) was induced by IL-23 stimulation. (b) IL-23 activated STAT3 signaling in both the CD117^-NKp44^- ILC1 and CD117⁺NKp44^- ILC3 subsets. (c) After gating Lin^-CD45⁺CD56⁺CD127⁺CRTH2^- ILCs, the tyrosine phosphorylation level of STAT3 was evaluated in ILCs. Donor with A/A genotype was shown in (A), and donor with G/G genotype was demonstrated in (B). The pSTAT3 level after 15 mins or 2 hrs stimulation of IL-23 indicated there was no delayed dephosphorylation in donors, suggesting risky allele “A” carriage does not affect the dephosphorylation of STAT3 in ILCs.

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