Figure 5. Adoptive transfer of Tregs reverses COX-2–KO–caused AT inflammation and insulin resistance.

For the following studies, mouse GFP⁺CD4⁺ T cells were isolated from lymph nodes and spleens of Foxp3-eGFP mice, and IP injection of CD4⁺GFP⁺ T cells which were positive Treg cells and CD4⁺GFP^- as negative control cells to 8 weeks HFD-fed COX-2–KO and control (Ctrl) mice. (A) There was little effect of adoptive transfer on the BW in COX-2–KO and control mice 2 weeks post transfer. Flow cytometry analysis of CD4⁺GFP⁺ cells (B), CD4⁺Foxp3⁺ Treg cells (C) and the proportion of Foxp3⁺ Treg in CD4⁺ cells (D) in eWAT showed the successful transfer of Tregs in AT. Adoptive transfer of Tregs increased CD11b⁺CD206⁺ cell fraction (E) and the proportion of CD11b⁺CD206⁺ in CD11b⁺ cells (F), while suppressed γδT⁺CD3⁺ cell population (G) and the proportion of γδT⁺CD3⁺ cell in total CD3⁺ cells (H). Adoptive transfer of Treg cells rescued COX-2 deficiency-induced glucose (I) and insulin (J) intolerance. *P < 0.05 and **P < 0.01 Ctrl vehicle (Veh) vs. Ctrl Treg; ^#P < 0.05 and ^##P < 0.01 for Ctrl Veh vs. KO Veh; ^$$P < 0.01 for KO Veh vs. KO Tregs; no significant difference was found between Ctrl Tregs and KO Tregs. (A–H) n = 4–7/group. (B) Representative data from 3 independent experiments are reported. ANOVA was used to analyze the data in this figure. Data are reported as mean ± SEM. *P < 0.05; **P < 0.01.