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. Author manuscript; available in PMC: 2022 Sep 15.
Published in final edited form as: J Immunol. 2021 Aug 20;207(6):1672–1682. doi: 10.4049/jimmunol.2100023

Figure 5: AHR agonism promotes an ILC1 phenotype in vivo.

Figure 5:

A) Schematic of in vivo studies. ILCPs (Lin-NKp80-CD294-KLRG1-NKp44-CD94−CD16−CD117+) and CD56bright NK cells (Lin-CD56+CD94+CD16−) were isolated from normal peripheral blood of 5 independent donors and adoptively transferred into NSG mice ± daily I.P. injections of FICZ (3 μg/mouse) or vehicle with biweekly injections of IL-7 and IL-15 for 4 weeks. At harvest, bone marrow was harvested and analyzed via flow cytometry for Group 1 human ILCs.

B) Representative flow plots of TBET and EOMES expression for human Lin-CD56+CD94+ cells derived from ILCPs or CD56bright NK cells ±FICZ.

C) Summary of ILC1:NK ratios comparing control conditions to FICZ-treated mice.

D) Summary data of TNFα and IFNγ expression determined by flow cytometry from ILCP- or CD56bright-derived NK cells and ILC1s from control or AML conditions.

n=3–5 (some mice excluded due to poor engraftment), *p<0.05. Error bars represent ±SEM.