Skip to main content
. Author manuscript; available in PMC: 2016 Apr 1.
Published in final edited form as: Gastroenterology. 2015 Jan 22;148(4):783–793.e5. doi: 10.1053/j.gastro.2015.01.027

Figure 6. TLR7 agonist R848 can overcome DC recruitment defect in SAMP mice.

Figure 6

(A) Migration of CD11c+MHCIIhi DC into MLN was measured 18h after gavage of R848 (0.5 μg/g). (B) Treatment induced migration of CD103+ CD11b+ and CD11b cells in the AKR mice. Percentages of parent gate ± SEM are indicated on the plots, # denotes significant differences between vehicle and R848 treated mice of the same strain. (C) Frequency of migratory cells at baseline (vehicle treated mice) and after TLR induction (R848) was lower in MLN of SAMP mice. n=5–6 in each group. (E) Activity of RA-synthesizing enzyme in CD11c+MHCIIhi MLN cells following TLR7 ligand treatment was measured by flow cytometry. Filled histograms show vehicle-treated mice, black open histograms depict R848-treated mice. Control sample treated with RALDH inhibitor DEAB is shown as gray open histograms. Data are representative of 3 experiments. **** p<0.0001, ** p<0.01, * p<0.05, # p<0.05 by two-sided Student’s t test