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. 2018 May;89:41–52. doi: 10.1016/j.jaut.2017.11.005

Fig. 1.

Fig. 1

Systemic antagomir-148a treatment of colitic mice depletes IFN-γ-expressing Th1 cells selectively in the inflamed colon. (A) Schematic overview depicting the experimental procedure for inducing colitis by adoptive transfer of repeatedly activated Th1 cells into Rag1−/− mice and subsequent antagomir treatment. (B) Representative dot plots showing the frequencies of CD3+CD4+ Th cells isolated from inflamed colons of colitic mice that were treated with antagomir-Scr or antagomir-148a. Displayed frequencies are percentages of Th cells among isolated viable cells. (C) Total cell numbers of viable CD3+CD4+ Th cells that were isolated from the colons and spleens of colitic mice following antagomir-148a or antagomir-Scr treatment as shown in (A). (D–G) Lymphocytes from colitic mice were isolated from the inflamed colons and stimulated with PMA/ionomycin in the presence of Brefeldin A. Shown are the absolute cell numbers of CD3+CD4+ Th cells that expressed IFN-γ (D), IL-10 (E), IL-17A (F) or IL-22 (G). (H) Quantification of different myeloid subsets isolated from inflamed colonic mucosae of colitic mice. Depicted data are pooled from two independent experiments with n = 12 and n = 13 for antagomir-148a- and antagomir-Scr-treated mice, respectively.