Journal: Science Advances
Article Title: 12R-HETE acts as an endogenous ligand for Nur77 in the intestines and regulates NKp46 + ILC3 development
doi: 10.1126/sciadv.adz8405
Figure Lengend Snippet: ( A ) Percentages of Ki67 + cells among RORγt + ILC3s are shown on the left. Absolute numbers of Ki67 + cells among RORγt + ILC3s are shown on the right. ( B ) Percentages of Ki67 + cells among NKp46 + ILC3s in the intestinal lamina propria. ( C ) Percentages of Ki67 + cells among NKp46 − ILC3s. ( D ) Numbers in flow plots represent percentages of T-bet + NKp46 + cells in the ILC3 gate. ( E ) Percentage of T-bet + cells among NKp46 + ILC3s. ( F ) IFN-γ MFI among NKp46 + ILC3s. ( G ) Percentage of T-bet + cells among DN ILC3s. ( H ) IFN-γ MFI among NKp46 + ILC3s. ( I ) Experimental design for the treatment of 12R-HETE and DAPT. SI LPLs were isolated from the 2-week-old mice. ( J ) Percentages and numbers of NKp46 + ILC3s were analyzed by flow cytometry after Notch signaling inhibitor treatment. ( K ) NKp46 MFI among NKp46 + ILC3. Data are means ± SEM; n = 5 to 6. Each point represents a biological replicate. * P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001; n.s., not significant.
Article Snippet: In mechanistic experiments, mice were intraperitoneally injected with Notch inhibitors DAPT [MedChemExpress (MCE)] or Impdh1 inhibitors MPA (MCE) after treatment with PBS or 12R-HETE, and animals were euthanized after 10 days.
Techniques: Isolation, Flow Cytometry