Skip to main content
. Author manuscript; available in PMC: 2011 Oct 22.
Published in final edited form as: Immunity. 2011 Apr 22;34(4):554–565. doi: 10.1016/j.immuni.2011.01.020

Figure 5. Tr1 cells suppress disease mediated by transfer of in vivo differentiated IL-17A+IFN-γ− and IL-17A+IFN-γ+ CD4+ T cells into Rag1−/− mice via IL-10.

Figure 5

IL-17A producing T cells were isolated from the colon and mLN as described in Figure S4. Tr1 cells were isolated from the small intestine of anti-CD3 treated mice and injected i.p. alone or together with IL-17A+ eGFP+ (IL-17A+) cells (WT or Cd4-DNIL-10R (Tg)) into Rag1−/− mice (A) Mass loss, (B) endoscopic and (C) histological colitis score were measured. Each dot represents one mouse. Lines indicate mean. (D) Representative endoscopic findings are shown. Note the bleeding (arrowhead), loss of transluceny, stool inconsistency (*), fibrin (**) and increased mucosal granularity (#) in the mice receiving IL-17A+ (WT), IL-17A+ (Tg) + Tr1 and IL-17A+ (Tg) cells. (E) Representative HE sections of colon are shown. The overall morphology in the colon of mice receiving IL-17A+ (WT)+Tr1 and Tr1 cells was not different from controls. Colons from mice receiving IL-17A+ (WT), IL-17A+ (Tg) + Tr1 and IL-17A+ (Tg) cells all had significant inflammation (*), crypt loss (arrowhead), edema (**), and moderate to marked mucosal hyperplasia (double arrows). HE Scale bars = 1000μm. Results are cumulative from 3 independent experiments.